=== Generating (published_papers) ===
=== Generating (teaching_experience) ===
=== Generating (education) ===
=== Generating (research_experience) ===
=== Generating (misc) ===
=== Generating (research_projects) ===
=== Generating (books_etc) ===
=== Generating (committee_memberships) ===
=== Generating (awards) ===
=== Generating (association_memberships) ===
=== Generating (presentations) ===
==== begin registerFile(/WWW/pub2/data/ERD/person/229223/researchmap/published_papers.jsonl) ====
line:1, {"insert":{"user_id":"B000337971","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/38883984","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=409654","label":"url"}],"paper_title":{"en":"Effects of renin-angiotensin system inhibitor and beta-blocker use on mortality in older patients with heart failure with reduced ejection fraction in Japan.","ja":"Effects of renin-angiotensin system inhibitor and beta-blocker use on mortality in older patients with heart failure with reduced ejection fraction in Japan."},"authors":{"en":[{"name":"Kawada Kei"},{"name":"Ishida Tomoaki"},{"name":"Fukuda Hitoshi"},{"name":"Hyohdoh Yuki"},{"name":"Kubo Toru"},{"name":"Hamada Tomoyuki"},{"name":"Baba Yuichi"},{"name":"Hayashi Toshinobu"},{"name":"Aizawa Fuka"},{"name":"Yagi Kenta"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Niimura Takahiro"},{"name":"Abe Shinji"},{"name":"Goda Mitsuhiro"},{"name":"Kitaoka Hiroaki"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"川田 敬"},{"name":"Ishida Tomoaki"},{"name":"Fukuda Hitoshi"},{"name":"Hyohdoh Yuki"},{"name":"Kubo Toru"},{"name":"Hamada Tomoyuki"},{"name":"Baba Yuichi"},{"name":"Hayashi Toshinobu"},{"name":"相澤 風花"},{"name":"八木 健太"},{"name":"石澤 有紀"},{"name":"新村 貴博"},{"name":"阿部 真治"},{"name":"合田 光寛"},{"name":"Kitaoka Hiroaki"},{"name":"石澤 啓介"}]},"description":{"en":"RAS inhibitors prevented all-cause mortality and cardiac death at all ages, whereas beta-blockers had different effects depending on the patient's age. This study suggested that the choice of beta-blockers and RAS inhibitors is more important in older patients with HFrEF than in younger patients with the same condition.","ja":"= 0.246, respectively). These results suggest that beta blockers may differ in their all-cause mortality benefits according to age."},"publication_date":"2024-05","publication_name":{"en":"Frontiers in Cardiovascular Medicine","ja":"Frontiers in Cardiovascular Medicine"},"volume":"Vol.11","languages":["eng"],"referee":true,"identifiers":{"doi":["10.3389/fcvm.2024.1377228"],"issn":["2297-055X"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:2, {"insert":{"user_id":"B000337971","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/38738173","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=409655","label":"url"}],"paper_title":{"en":"Atractylodes lancea (Thunb.) DC. [Asteraceae] rhizome-derived exosome-like nanoparticles suppress lipopolysaccharide-induced inflammation in murine microglial cells.","ja":"Atractylodes lancea (Thunb.) DC. [Asteraceae] rhizome-derived exosome-like nanoparticles suppress lipopolysaccharide-induced inflammation in murine microglial cells."},"authors":{"en":[{"name":"Kawada Kei"},{"name":"Ishida Tomoaki"},{"name":"Morisawa Shumpei"},{"name":"Jobu Kohei"},{"name":"Higashi Youichirou"},{"name":"Aizawa Fuka"},{"name":"Yagi Kenta"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Niimura Takahiro"},{"name":"Abe Shinji"},{"name":"Goda Mitsuhiro"},{"name":"Miyamura Mitsuhiko"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"川田 敬"},{"name":"Ishida Tomoaki"},{"name":"Morisawa Shumpei"},{"name":"Jobu Kohei"},{"name":"Higashi Youichirou"},{"name":"相澤 風花"},{"name":"八木 健太"},{"name":"石澤 有紀"},{"name":"新村 貴博"},{"name":"阿部 真治"},{"name":"合田 光寛"},{"name":"Miyamura Mitsuhiko"},{"name":"石澤 啓介"}]},"description":{"en":"Exosome-like nanoparticles (ELNs) mediate interspecies intercellular communications and modulate gene expression. In this study, we isolated and purified ELNs from the dried rhizome of Atractylodes lancea (Thunb.) DC. [Asteraceae] (ALR-ELNs), a traditional natural medicine, and investigated their potential as neuroinflammatory therapeutic agents. ALR-ELN samples were isolated and purified using differential centrifugation, and their physical features and microRNA contents were analyzed through transmission electron microscopy and RNA sequencing, respectively. BV-2 microglial murine cells and primary mouse microglial cells were cultured , and their ability to uptake ALR-ELNs was explored using fluorescence microscopy. The capacity of ALR-ELNs to modulate the anti-inflammatory responses of these cells to lipopolysaccharide (LPS) exposure was assessed through mRNA and protein expression analyses. Overall, BV-2 cells were found to internalize ALR-ELNs, which comprised three microRNAs (ath-miR166f, ath-miR162a-5p, and ath-miR162b-5p) that could have anti-inflammatory activity. Pretreatment of BV-2 cells with ALR-ELN prevented the pro-inflammatory effects of LPS stimulation by significantly reducing the levels of nitric oxide, interleukin-1β, interleukin-6, and tumor necrosis factor-α. Notably, the mRNA levels of , and in BV-2 cells, which increased upon LPS exposure, were significantly reduced following ALR-ELN treatment. Moreover, the mRNA levels of heme oxygenase 1, , and also increased significantly following ALR-ELN treatment. In addition, pretreatment of primary mouse microglial cells with ALR-ELN prevented the pro-inflammatory effects of LPS stimulation by significantly reducing the levels of nitric oxide. Our findings indicate that ALR-ELNs exhibit anti-inflammatory effects on murine microglial cells. Further validation may prove ALR-ELNs as a promising neuroinflammatory therapeutic agent.","ja":"Exosome-like nanoparticles (ELNs) mediate interspecies intercellular communications and modulate gene expression. In this study, we isolated and purified ELNs from the dried rhizome of Atractylodes lancea (Thunb.) DC. [Asteraceae] (ALR-ELNs), a traditional natural medicine, and investigated their potential as neuroinflammatory therapeutic agents. ALR-ELN samples were isolated and purified using differential centrifugation, and their physical features and microRNA contents were analyzed through transmission electron microscopy and RNA sequencing, respectively. BV-2 microglial murine cells and primary mouse microglial cells were cultured , and their ability to uptake ALR-ELNs was explored using fluorescence microscopy. The capacity of ALR-ELNs to modulate the anti-inflammatory responses of these cells to lipopolysaccharide (LPS) exposure was assessed through mRNA and protein expression analyses. Overall, BV-2 cells were found to internalize ALR-ELNs, which comprised three microRNAs (ath-miR166f, ath-miR162a-5p, and ath-miR162b-5p) that could have anti-inflammatory activity. Pretreatment of BV-2 cells with ALR-ELN prevented the pro-inflammatory effects of LPS stimulation by significantly reducing the levels of nitric oxide, interleukin-1β, interleukin-6, and tumor necrosis factor-α. Notably, the mRNA levels of , and in BV-2 cells, which increased upon LPS exposure, were significantly reduced following ALR-ELN treatment. Moreover, the mRNA levels of heme oxygenase 1, , and also increased significantly following ALR-ELN treatment. In addition, pretreatment of primary mouse microglial cells with ALR-ELN prevented the pro-inflammatory effects of LPS stimulation by significantly reducing the levels of nitric oxide. Our findings indicate that ALR-ELNs exhibit anti-inflammatory effects on murine microglial cells. Further validation may prove ALR-ELNs as a promising neuroinflammatory therapeutic agent."},"publication_date":"2024-04-26","publication_name":{"en":"Frontiers in Pharmacology","ja":"Frontiers in Pharmacology"},"volume":"Vol.15","languages":["eng"],"referee":true,"identifiers":{"doi":["10.3389/fphar.2024.1302055"],"issn":["1663-9812"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:3, {"insert":{"user_id":"B000337971","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=415126","label":"url"}],"paper_title":{"en":"Statins ameliorate oxaliplatin- and paclitaxel-induced peripheral neuropathy via glutathione-S-transferase","ja":"Statins ameliorate oxaliplatin- and paclitaxel-induced peripheral neuropathy via glutathione-S-transferase"},"authors":{"en":[{"name":"Aizawa Fuka"},{"name":"Kajimoto Haruna"},{"name":"Ami Okabayashi"},{"name":"Moriyama Daishi"},{"name":"Yagi Kenta"},{"name":"Shimon Takahashi"},{"name":"Yuhei sonoda"},{"name":"Takahiro shibata"},{"name":"Goda Mitsuhiro"},{"name":"Niimura Takahiro"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Hamano Hirofumi"},{"name":"Kawada Kei"},{"name":"Zamami Yoshito"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"相澤 風花"},{"name":"梶本 春奈"},{"name":"岡林 亜美"},{"name":"森山 大嗣"},{"name":"八木 健太"},{"name":"高橋 志門"},{"name":"薗田 悠平"},{"name":"柴田 高洋"},{"name":"合田 光寛"},{"name":"新村 貴博"},{"name":"石澤 有紀"},{"name":"濱野 裕章"},{"name":"川田 敬"},{"name":"座間味 義人"},{"name":"石澤 啓介"}]},"publication_date":"2024","publication_name":{"en":"Neurochemistry International","ja":"Neurochemistry International"},"volume":"Vol.180","starting_page":"105863","ending_page":"105863","languages":["eng"],"referee":true,"identifiers":{"issn":["0197-0186"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:4, {"insert":{"user_id":"B000337971","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=415119","label":"url"}],"paper_title":{"en":"A Novel Allosteric Inhibitor of BCR-ABL1, Shows Synergistic Effects When Used in Combination with Imatinib with or without Drug Resistance.","ja":"A Novel Allosteric Inhibitor of BCR-ABL1, Shows Synergistic Effects When Used in Combination with Imatinib with or without Drug Resistance."},"authors":{"en":[{"name":"Naoki Okamoto"},{"name":"Yagi Kenta"},{"name":"Sayaka Imawaka"},{"name":"Mayu Takaoka"},{"name":"Aizawa Fuka"},{"name":"Niimura Takahiro"},{"name":"Goda Mitsuhiro"},{"name":"Koji Miyata"},{"name":"Kawada Kei"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Sakaguchi Satoshi"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"岡本 尚大"},{"name":"八木 健太"},{"name":"今若 清香"},{"name":"髙岡 麻佑"},{"name":"相澤 風花"},{"name":"新村 貴博"},{"name":"合田 光寛"},{"name":"宮田 晃志"},{"name":"川田 敬"},{"name":"石澤 有紀"},{"name":"坂口 暁"},{"name":"石澤 啓介"}]},"publication_date":"2024","publication_name":{"en":"Pharmacology Research & Perspectives","ja":"Pharmacology Research & Perspectives"},"volume":"Vol.12","number":"No.4","starting_page":"e1214","ending_page":"e1214","languages":["eng"],"referee":true,"identifiers":{"issn":["2052-1707"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:5, {"insert":{"user_id":"B000337971","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/118742","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/38145933","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=407553","label":"url"}],"paper_title":{"en":"Concomitant Use of Multiple Nephrotoxins including Renal Hypoperfusion Medications Causes Vancomycin-Associated Nephrotoxicity: Combined Retrospective Analyses of Two Real-World Databases.","ja":"Concomitant Use of Multiple Nephrotoxins including Renal Hypoperfusion Medications Causes Vancomycin-Associated Nephrotoxicity: Combined Retrospective Analyses of Two Real-World Databases."},"authors":{"en":[{"name":"Bando Takashi"},{"name":"Chuma Masayuki"},{"name":"Hamano Hirofumi"},{"name":"Niimura Takahiro"},{"name":"Okada Naoto"},{"name":"Kondo Masateru"},{"name":"Izumi Yuki"},{"name":"Ishida Shunsuke"},{"name":"Yoshioka Toshihiko"},{"name":"Asada Mizuho"},{"name":"Zamami Yoshito"},{"name":"Takechi Kenshi"},{"name":"Goda Mitsuhiro"},{"name":"Miyata Koji"},{"name":"Yagi Kenta"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Azuma Momoyo"},{"name":"Yanagawa Hiroaki"},{"name":"Tasaki Yoshikazu"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"坂東 貴司"},{"name":"中馬 真幸"},{"name":"濱野 裕章"},{"name":"新村 貴博"},{"name":"岡田 直人"},{"name":"近藤 正輝"},{"name":"泉 侑希"},{"name":"石田 俊介"},{"name":"吉岡 俊彦"},{"name":"朝田 瑞穂"},{"name":"座間味 義人"},{"name":"武智 研志"},{"name":"合田 光寛"},{"name":"宮田 晃志"},{"name":"八木 健太"},{"name":"石澤 有紀"},{"name":"東 桃代"},{"name":"楊河 宏章"},{"name":"田崎 嘉一"},{"name":"石澤 啓介"}]},"description":{"en":"There is a growing concern about the relationship between vancomycin-associated nephrotoxicity (VAN) and concomitant use of nephrotoxins. We examined this relationship by combined retrospective analyses of two real-world databases. Initially, the FDA Adverse Event Reporting System (FAERS) was analyzed for the effects of concomitant use of one or more nephrotoxins on VAN and the types of combinations of nephrotoxins that exacerbate VAN. Next, electronic medical records (EMRs) of patients who received vancomycin (VCM) at Tokushima University Hospital between January 2006 and March 2019 were examined to confirm the FAERS analysis. An elevated reporting odds ratio (ROR) was observed with increases in the number of nephrotoxins administered (VCM + one nephrotoxin, adjusted ROR (95% confidence interval [CI]) 1.67 [1.51-1.85]; VCM + 2 nephrotoxins, adjusted ROR [95% CI] 1.54 [1.37-1.73]) in FAERS. EMRs analysis showed that the number of nephrotoxins was associated with higher incidences of VAN [odds ratio: 1.99; 95% CI: 1.42-2.78]. Overall, concomitant use of nephrotoxins was associated with an increased incidence of VAN, especially when at least one of those nephrotoxins was a renal hypoperfusion medication (furosemide, non-steroidal anti-inflammatory drugs, and vasopressors). The concomitant use of multiple nephrotoxins, especially including renal hypoperfusion medication, should be avoided to prevent VAN.","ja":"There is a growing concern about the relationship between vancomycin-associated nephrotoxicity (VAN) and concomitant use of nephrotoxins. We examined this relationship by combined retrospective analyses of two real-world databases. Initially, the FDA Adverse Event Reporting System (FAERS) was analyzed for the effects of concomitant use of one or more nephrotoxins on VAN and the types of combinations of nephrotoxins that exacerbate VAN. Next, electronic medical records (EMRs) of patients who received vancomycin (VCM) at Tokushima University Hospital between January 2006 and March 2019 were examined to confirm the FAERS analysis. An elevated reporting odds ratio (ROR) was observed with increases in the number of nephrotoxins administered (VCM + one nephrotoxin, adjusted ROR (95% confidence interval [CI]) 1.67 [1.51-1.85]; VCM + 2 nephrotoxins, adjusted ROR [95% CI] 1.54 [1.37-1.73]) in FAERS. EMRs analysis showed that the number of nephrotoxins was associated with higher incidences of VAN [odds ratio: 1.99; 95% CI: 1.42-2.78]. Overall, concomitant use of nephrotoxins was associated with an increased incidence of VAN, especially when at least one of those nephrotoxins was a renal hypoperfusion medication (furosemide, non-steroidal anti-inflammatory drugs, and vasopressors). The concomitant use of multiple nephrotoxins, especially including renal hypoperfusion medication, should be avoided to prevent VAN."},"publication_date":"2023-12","publication_name":{"en":"Acta Medica Okayama","ja":"Acta Medica Okayama"},"volume":"Vol.77","number":"No.6","starting_page":"595","ending_page":"605","languages":["eng"],"referee":true,"identifiers":{"doi":["10.18926/AMO/66151"],"issn":["0386-300X"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:6, {"insert":{"user_id":"B000337971","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/118743","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/37700528","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=407554","label":"url"}],"paper_title":{"en":"Valproic acid treatment attenuates cisplatin-induced kidney injury by suppressing proximal tubular cell damage.","ja":"Valproic acid treatment attenuates cisplatin-induced kidney injury by suppressing proximal tubular cell damage."},"authors":{"en":[{"name":"Yoshioka Toshihiko"},{"name":"Goda Mitsuhiro"},{"name":"Kanda Masaya"},{"name":"Itobayashi Sayuri"},{"name":"Sugimoto Yugo"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Yagi Kenta"},{"name":"Aizawa Fuka"},{"name":"Miyata Koji"},{"name":"Niimura Takahiro"},{"name":"Hamano Hirofumi"},{"name":"Sakurada Takumi"},{"name":"Zamami Yoshito"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"吉岡 俊彦"},{"name":"合田 光寛"},{"name":"神田 将哉"},{"name":"糸林 小友理"},{"name":"杉本 祐悟"},{"name":"石澤 有紀"},{"name":"八木 健太"},{"name":"相澤 風花"},{"name":"宮田 晃志"},{"name":"新村 貴博"},{"name":"濱野 裕章"},{"name":"櫻田 巧"},{"name":"座間味 義人"},{"name":"石澤 啓介"}]},"description":{"en":"Cisplatin treatment is effective against several types of carcinomas. However, it frequently leads to kidney injury, which warrants effective prevention methods. Sodium valproic acid is a prophylactic drug candidate with a high potential for clinical application against cisplatin-induced kidney injury. Therefore, in this study, we aimed to elucidate the mechanism underlying the prophylactic effect of valproic acid on cisplatin-induced kidney injury in a mouse model and HK2 and PODO cells with cisplatin-induced toxicity. In the mouse model of cisplatin-induced kidney injury, various renal function parameters and tubular damage scores were worsened by cisplatin, but they were significantly improved upon combination with valproic acid. No difference was observed in cisplatin accumulation between the cisplatin-treated and valproic acid-treated groups in whole blood and the kidneys. The mRNA expression levels of proximal tubular damage markers, apoptosis markers, and inflammatory cytokines significantly increased in the cisplatin group 72 h after cisplatin administration but significantly decreased upon combination with valproic acid. In HK2 cells, a human proximal tubular cell line, the cisplatin-induced decrease in cell viability was significantly suppressed by co-treatment with valproic acid. Valproic acid may inhibit cisplatin-induced kidney injury by suppressing apoptosis, inflammatory responses, and glomerular damage throughout the kidneys by suppressing proximal tubular cell damage. However, prospective controlled trials need to evaluate these findings before their practical application.","ja":"Cisplatin treatment is effective against several types of carcinomas. However, it frequently leads to kidney injury, which warrants effective prevention methods. Sodium valproic acid is a prophylactic drug candidate with a high potential for clinical application against cisplatin-induced kidney injury. Therefore, in this study, we aimed to elucidate the mechanism underlying the prophylactic effect of valproic acid on cisplatin-induced kidney injury in a mouse model and HK2 and PODO cells with cisplatin-induced toxicity. In the mouse model of cisplatin-induced kidney injury, various renal function parameters and tubular damage scores were worsened by cisplatin, but they were significantly improved upon combination with valproic acid. No difference was observed in cisplatin accumulation between the cisplatin-treated and valproic acid-treated groups in whole blood and the kidneys. The mRNA expression levels of proximal tubular damage markers, apoptosis markers, and inflammatory cytokines significantly increased in the cisplatin group 72 h after cisplatin administration but significantly decreased upon combination with valproic acid. In HK2 cells, a human proximal tubular cell line, the cisplatin-induced decrease in cell viability was significantly suppressed by co-treatment with valproic acid. Valproic acid may inhibit cisplatin-induced kidney injury by suppressing apoptosis, inflammatory responses, and glomerular damage throughout the kidneys by suppressing proximal tubular cell damage. However, prospective controlled trials need to evaluate these findings before their practical application."},"publication_date":"2023-09-25","publication_name":{"en":"Clinical and Translational Science","ja":"Clinical and Translational Science"},"volume":"Vol.16","number":"No.11","starting_page":"2369","ending_page":"2381","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1111/cts.13638"],"issn":["1752-8062"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:7, {"insert":{"user_id":"B000337971","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/119327","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/37722188","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=406562","label":"url"}],"paper_title":{"en":"Angiogenesis inhibitor-specific hypertension increases the risk of developing aortic dissection.","ja":"Angiogenesis inhibitor-specific hypertension increases the risk of developing aortic dissection."},"authors":{"en":[{"name":"Tsujinaka Kaito"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Miyata Koji"},{"name":"Yoshioka Toshihiko"},{"name":"Oomine Kohei"},{"name":"Nishi Honoka"},{"name":"Kondo Masateru"},{"name":"Itokazu Syuto"},{"name":"Miyata Tatsumi"},{"name":"Niimura Takahiro"},{"name":"Sato Maki"},{"name":"Aizawa Fuka"},{"name":"Yagi Kenta"},{"name":"Chuma Masayuki"},{"name":"Zamami Yoshito"},{"name":"Goda Mitsuhiro"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"Tsujinaka Kaito"},{"name":"石澤 有紀"},{"name":"Miyata Koji"},{"name":"Yoshioka Toshihiko"},{"name":"Oomine Kohei"},{"name":"Nishi Honoka"},{"name":"Kondo Masateru"},{"name":"Itokazu Syuto"},{"name":"Miyata Tatsumi"},{"name":"新村 貴博"},{"name":"Sato Maki"},{"name":"相澤 風花"},{"name":"八木 健太"},{"name":"中馬 真幸"},{"name":"座間味 義人"},{"name":"合田 光寛"},{"name":"石澤 啓介"}]},"description":{"en":"Aortic dissection is an adverse event of angiogenesis inhibitors; however, the association between the drugs and aortic dissection is unclear. Therefore, we investigated if and how angiogenesis inhibitors increase the onset of aortic dissection using pharmacologically-induced aortic dissection-prone model (LAB) mice, cultured endothelial cells, and real-world databases, which is a novel integrated research approach. Disproportionality analysis was performed and calculated using the reporting odds ratio as a risk signal using a worldwide database of spontaneous adverse events to estimate the risk of adverse events. Angiogenesis inhibitors, but not other hypertension-inducing drugs, showed significant risk signals for aortic aneurysms and dissection. A retrospective cohort analysis using JMDC, a medical receipt database in Japan, showed that the history of atherosclerosis and dyslipidemia, but not hypertension, were significantly associated with the onset of aortic dissection during angiogenesis inhibitor medication administration. For in vivo studies, sunitinib (100 mg/kg/day) was administered to LAB mice. Sunitinib increased systolic blood pressure (182 mmHg vs. 288 mmHg with sunitinib; p<0.01) and the incidence of aortic dissection (40% vs. 59% with sunitinib; p = 0.34) in mice. In vivo and in vitro studies revealed that sunitinib increased endothelin-1 expression and induced endothelial cell damage evaluated by intracellular- and vascular cell adhesion molecule-1 expressions. The increased risk of developing aortic dissection with angiogenesis inhibitors is associated with the development of drug-specific hypertension via endothelial cell damage and endothelin-1 expression. Our findings are invaluable in establishing safer anticancer therapies and strategies to prevent the development of vascular toxicity in high-risk patients.","ja":"Aortic dissection is an adverse event of angiogenesis inhibitors; however, the association between the drugs and aortic dissection is unclear. Therefore, we investigated if and how angiogenesis inhibitors increase the onset of aortic dissection using pharmacologically-induced aortic dissection-prone model (LAB) mice, cultured endothelial cells, and real-world databases, which is a novel integrated research approach. Disproportionality analysis was performed and calculated using the reporting odds ratio as a risk signal using a worldwide database of spontaneous adverse events to estimate the risk of adverse events. Angiogenesis inhibitors, but not other hypertension-inducing drugs, showed significant risk signals for aortic aneurysms and dissection. A retrospective cohort analysis using JMDC, a medical receipt database in Japan, showed that the history of atherosclerosis and dyslipidemia, but not hypertension, were significantly associated with the onset of aortic dissection during angiogenesis inhibitor medication administration. For in vivo studies, sunitinib (100 mg/kg/day) was administered to LAB mice. Sunitinib increased systolic blood pressure (182 mmHg vs. 288 mmHg with sunitinib; p<0.01) and the incidence of aortic dissection (40% vs. 59% with sunitinib; p = 0.34) in mice. In vivo and in vitro studies revealed that sunitinib increased endothelin-1 expression and induced endothelial cell damage evaluated by intracellular- and vascular cell adhesion molecule-1 expressions. The increased risk of developing aortic dissection with angiogenesis inhibitors is associated with the development of drug-specific hypertension via endothelial cell damage and endothelin-1 expression. Our findings are invaluable in establishing safer anticancer therapies and strategies to prevent the development of vascular toxicity in high-risk patients."},"publication_date":"2023-09-16","publication_name":{"en":"Biomedicine & Pharmacotherapy","ja":"Biomedicine & Pharmacotherapy"},"volume":"Vol.167","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1016/j.biopha.2023.115504"],"issn":["1950-6007"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:8, {"insert":{"user_id":"B000337971","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/37106270","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=396451","label":"url"}],"paper_title":{"en":"Cardiovascular Toxicities Associated with Anaplastic Lymphoma Kinase Inhibitors: A Disproportionality Analysis of the WHO Pharmacovigilance Database (VigiBase).","ja":"Cardiovascular Toxicities Associated with Anaplastic Lymphoma Kinase Inhibitors: A Disproportionality Analysis of the WHO Pharmacovigilance Database (VigiBase)."},"authors":{"en":[{"name":"Niimura Takahiro"},{"name":"Miyata Koji"},{"name":"Hamano Hirofumi"},{"name":"Nounin Yuuki"},{"name":"Unten Hiroto"},{"name":"Yoshino Masaki"},{"name":"Mitsuboshi Satoru"},{"name":"Aizawa Fuka"},{"name":"Yagi Kenta"},{"name":"Koyama Toshihiro"},{"name":"Goda Mitsuhiro"},{"name":"Kanda Yasunari"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Zamami Yoshito"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"新村 貴博"},{"name":"宮田 晃志"},{"name":"濱野 裕章"},{"name":"Nounin Yuuki"},{"name":"運天 拡人"},{"name":"Yoshino Masaki"},{"name":"Mitsuboshi Satoru"},{"name":"相澤 風花"},{"name":"八木 健太"},{"name":"Koyama Toshihiro"},{"name":"合田 光寛"},{"name":"Kanda Yasunari"},{"name":"石澤 有紀"},{"name":"座間味 義人"},{"name":"石澤 啓介"}]},"description":{"en":"Systematic evaluation of ALK inhibitor-associated adverse events revealed differences in the cardiotoxicity profiles among ALK inhibitors. Understanding the differences in the cardiovascular toxicity profile of each ALK inhibitor will contribute to safe drug therapy when switching between ALK inhibitors.","ja":"Systematic evaluation of ALK inhibitor-associated adverse events revealed differences in the cardiotoxicity profiles among ALK inhibitors. Understanding the differences in the cardiovascular toxicity profile of each ALK inhibitor will contribute to safe drug therapy when switching between ALK inhibitors."},"publication_date":"2023-04-27","publication_name":{"en":"Drug Safety","ja":"Drug Safety"},"languages":["eng"],"referee":true,"identifiers":{"doi":["10.1007/s40264-023-01300-9"],"issn":["1179-1942"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:9, {"insert":{"user_id":"B000337971","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/36738305","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=394581","label":"url"}],"paper_title":{"en":"Effects of vonoprazan and proton pump inhibitors on the efficacy of bevacizumab: a multicentre retrospective study.","ja":"Effects of vonoprazan and proton pump inhibitors on the efficacy of bevacizumab: a multicentre retrospective study."},"authors":{"en":[{"name":"Yagi Kenta"},{"name":"Maruo Akinori"},{"name":"Ishida Shunsuke"},{"name":"Aizawa Fuka"},{"name":"Ushio Soichiro"},{"name":"Sakaguchi Satoshi"},{"name":"Kajizono Makoto"},{"name":"Niimura Takahiro"},{"name":"Goda Mitsuhiro"},{"name":"Hamano Hirofumi"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Zamami Yoshito"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"八木 健太"},{"name":"Maruo Akinori"},{"name":"Ishida Shunsuke"},{"name":"相澤 風花"},{"name":"Ushio Soichiro"},{"name":"坂口 暁"},{"name":"Kajizono Makoto"},{"name":"新村 貴博"},{"name":"合田 光寛"},{"name":"濱野 裕章"},{"name":"石澤 有紀"},{"name":"座間味 義人"},{"name":"石澤 啓介"}]},"description":{"en":"Gastric acid secretion inhibitors such as proton pump inhibitors (PPIs) and vonoprazan may change the duration of treatment with bevacizumab, a vascular endothelial growth factor (VEGF) inhibitor, for cancer. However, there are no data on this prolongation effect. Here, we aimed to determine whether the use of PPIs or vonoprazan in patients with cancer receiving bevacizumab affected the duration of bevacizumab treatment. This observational study was conducted at two national university hospitals in Japan and involved 222 patients using oral PPIs (N = 190) or vonoprazan (N = 32) at the start of bevacizumab treatment between January 2015 and December 2018. Patients who received only one course of bevacizumab were excluded. The primary endpoint was the duration of bevacizumab treatment. The duration of bevacizumab treatment varied significantly between the PPI and vonoprazan groups. For cancer types other than colorectal cancer (breast, lung, brain, and ovarian cancers), the median duration of treatment was 217 days (p < 0.05) and was longer in the vonoprazan group than in the PPI group. However, for colorectal cancer, the median duration of bevacizumab treatment was 147 days longer in the PPI group than in the vonoprazan group. Selection of appropriate gastric acid secretion inhibitors may improve the therapeutic efficacy of anti-VEGF drugs, including bevacizumab. Oestrogen is a key regulator of this effect and may be responsible for the varying association between PPI or vonoprazan administration and the difference in bevacizumab treatment duration between colon cancer and other cancer types.","ja":"Gastric acid secretion inhibitors such as proton pump inhibitors (PPIs) and vonoprazan may change the duration of treatment with bevacizumab, a vascular endothelial growth factor (VEGF) inhibitor, for cancer. However, there are no data on this prolongation effect. Here, we aimed to determine whether the use of PPIs or vonoprazan in patients with cancer receiving bevacizumab affected the duration of bevacizumab treatment. This observational study was conducted at two national university hospitals in Japan and involved 222 patients using oral PPIs (N = 190) or vonoprazan (N = 32) at the start of bevacizumab treatment between January 2015 and December 2018. Patients who received only one course of bevacizumab were excluded. The primary endpoint was the duration of bevacizumab treatment. The duration of bevacizumab treatment varied significantly between the PPI and vonoprazan groups. For cancer types other than colorectal cancer (breast, lung, brain, and ovarian cancers), the median duration of treatment was 217 days (p < 0.05) and was longer in the vonoprazan group than in the PPI group. However, for colorectal cancer, the median duration of bevacizumab treatment was 147 days longer in the PPI group than in the vonoprazan group. Selection of appropriate gastric acid secretion inhibitors may improve the therapeutic efficacy of anti-VEGF drugs, including bevacizumab. Oestrogen is a key regulator of this effect and may be responsible for the varying association between PPI or vonoprazan administration and the difference in bevacizumab treatment duration between colon cancer and other cancer types."},"publication_date":"2023-02-04","publication_name":{"en":"Clinical and Experimental Medicine","ja":"Clinical and Experimental Medicine"},"languages":["eng"],"referee":true,"identifiers":{"doi":["10.1007/s10238-023-01008-1"],"issn":["1591-9528"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:10, {"insert":{"user_id":"B000337971","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/36453166","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=396493","label":"url"}],"paper_title":{"en":"Characterization of Immune Checkpoint Inhibitor-Induced Myasthenia Gravis Using the US Food and Drug Administration Adverse Event Reporting System.","ja":"Characterization of Immune Checkpoint Inhibitor-Induced Myasthenia Gravis Using the US Food and Drug Administration Adverse Event Reporting System."},"authors":{"en":[{"name":"Niimura Takahiro"},{"name":"Zamami Yoshito"},{"name":"Miyata Koji"},{"name":"Mikami Takahisa"},{"name":"Asada Mizuho"},{"name":"Fukushima Keijo"},{"name":"Yoshino Masaki"},{"name":"Mitsuboshi Satoru"},{"name":"Okada Naoto"},{"name":"Hamano Hirofumi"},{"name":"Sakurada Takumi"},{"name":"Matsuoka-Ando Rie"},{"name":"Aizawa Fuka"},{"name":"Yagi Kenta"},{"name":"Goda Mitsuhiro"},{"name":"Chuma Masayuki"},{"name":"Koyama Toshihiro"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Yanagawa Hiroaki"},{"name":"Fujino Hiromichi"},{"name":"Yamanishi Yoshihiro"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"新村 貴博"},{"name":"座間味 義人"},{"name":"宮田 晃志"},{"name":"Mikami Takahisa"},{"name":"Asada Mizuho"},{"name":"福島 圭穣"},{"name":"Yoshino Masaki"},{"name":"Mitsuboshi Satoru"},{"name":"岡田 直人"},{"name":"濱野 裕章"},{"name":"櫻田 巧"},{"name":"Matsuoka-Ando Rie"},{"name":"相澤 風花"},{"name":"八木 健太"},{"name":"合田 光寛"},{"name":"中馬 真幸"},{"name":"Koyama Toshihiro"},{"name":"石澤 有紀"},{"name":"楊河 宏章"},{"name":"藤野 裕道"},{"name":"Yamanishi Yoshihiro"},{"name":"石澤 啓介"}]},"description":{"en":"Myasthenia gravis (MG) is a rare but fatal adverse event of immune checkpoint inhibitors (ICIs). We assessed whether patient characteristics differed between those with ICI-related myasthenia gravis and those with idiopathic myasthenia gravis. Reports from the US Food and Drug Administration Adverse Event Reporting System were analyzed. Multivariate analyses were conducted to evaluate the associations between age, sex, and ICI treatment and the reporting rate of myasthenia gravis. Among 5 464 099 cases between 2011 and 2019, 53 447 were treated with ICIs. Myasthenia gravis was reported more often in ICI users. Multiple logistic regression analyses showed that the reporting rate of ICI-related myasthenia gravis did not differ significantly between men and women; however, it was higher in older people than in younger people (adjusted odds ratio, 2.4 [95%CI, 1.84-3.13]). We also investigated useful signs for the early detection of myositis and myocarditis, which are fatal when overlapping with ICI-related myasthenia gravis. Patients with elevated serum creatine kinase or troponin levels were more likely to have concurrent myositis and myocarditis. Unlike idiopathic myasthenia gravis, there was no sex difference in the development of ICI-related myasthenia gravis, which may be more common in older people. Considering the physiological muscle weakness that occurs in the elderly, it may be necessary to monitor ICI-related myasthenia gravis more closely in older people.","ja":"Myasthenia gravis (MG) is a rare but fatal adverse event of immune checkpoint inhibitors (ICIs). We assessed whether patient characteristics differed between those with ICI-related myasthenia gravis and those with idiopathic myasthenia gravis. Reports from the US Food and Drug Administration Adverse Event Reporting System were analyzed. Multivariate analyses were conducted to evaluate the associations between age, sex, and ICI treatment and the reporting rate of myasthenia gravis. Among 5 464 099 cases between 2011 and 2019, 53 447 were treated with ICIs. Myasthenia gravis was reported more often in ICI users. Multiple logistic regression analyses showed that the reporting rate of ICI-related myasthenia gravis did not differ significantly between men and women; however, it was higher in older people than in younger people (adjusted odds ratio, 2.4 [95%CI, 1.84-3.13]). We also investigated useful signs for the early detection of myositis and myocarditis, which are fatal when overlapping with ICI-related myasthenia gravis. Patients with elevated serum creatine kinase or troponin levels were more likely to have concurrent myositis and myocarditis. Unlike idiopathic myasthenia gravis, there was no sex difference in the development of ICI-related myasthenia gravis, which may be more common in older people. Considering the physiological muscle weakness that occurs in the elderly, it may be necessary to monitor ICI-related myasthenia gravis more closely in older people."},"publication_date":"2022-12-21","publication_name":{"en":"Journal of Clinical Pharmacology","ja":"Journal of Clinical Pharmacology"},"volume":"Vol.63","number":"No.4","starting_page":"473","ending_page":"479","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1002/jcph.2187"],"issn":["1552-4604"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:11, {"insert":{"user_id":"B000337971","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/118289","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/36484282","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=394580","label":"url"}],"paper_title":{"en":"Differential effects of proton pump inhibitors and vonoprazan on vascular endothelial growth factor expression in cancer cells.","ja":"Differential effects of proton pump inhibitors and vonoprazan on vascular endothelial growth factor expression in cancer cells."},"authors":{"en":[{"name":"Ando-Matsuoka Rie"},{"name":"Yagi Kenta"},{"name":"Takaoka Mayu"},{"name":"Sakajiri Yuko"},{"name":"Shibata Tomokazu"},{"name":"Sawada Ryusuke"},{"name":"Maruo Akinori"},{"name":"Miyata Koji"},{"name":"Aizawa Fuka"},{"name":"Hamano Hirofumi"},{"name":"Niimura Takahiro"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Goda Mitsuhiro"},{"name":"Sakaguchi Satoshi"},{"name":"Zamami Yoshito"},{"name":"Yamanishi Yoshihiro"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"Ando-Matsuoka Rie"},{"name":"八木 健太"},{"name":"Takaoka Mayu"},{"name":"Sakajiri Yuko"},{"name":"Shibata Tomokazu"},{"name":"Sawada Ryusuke"},{"name":"Maruo Akinori"},{"name":"Miyata Koji"},{"name":"相澤 風花"},{"name":"濱野 裕章"},{"name":"新村 貴博"},{"name":"石澤 有紀"},{"name":"合田 光寛"},{"name":"坂口 暁"},{"name":"座間味 義人"},{"name":"Yamanishi Yoshihiro"},{"name":"石澤 啓介"}]},"description":{"en":"Proton pump inhibitors (PPIs) are potent inhibitors of gastric acid secretion, used as first-line agents in treating peptic ulcers. However, we have previously reported that PPIs may diminish the therapeutic effect of anti-vascular endothelial growth factor (VEGF) drugs in patients with cancer. In this study, we explored the effects of vonoprazan, a novel gastric acid secretion inhibitor used for the treatment of peptic ulcers, on the secretion of VEGF in cancer cells and attempted to propose it as an alternative PPI for cancer chemotherapy. The effects of PPI and vonoprazan on VEGF expression in cancer cells were compared by real-time reverse transcription-polymerase chain reaction and ELISA. The interaction of vonoprazan and PPIs with transcriptional regulators by docking simulation analysis. In various cancer cell lines, including the human colorectal cancer cell line (LS174T), PPI increased VEGF messenger RNA expression and VEGF protein secretion, while this effect was not observed with vonoprazan. Molecular docking simulation analysis showed that vonoprazan had a lower binding affinity for estrogen receptor alpha (ER-α), one of the transcriptional regulators of VEGF, compared to PPI. Although the PPI-induced increase in VEGF expression was counteracted by pharmacological ER-α inhibition, the effect of vonoprazan on VEGF expression was unchanged. Vonoprazan does not affect VEGF expression in cancer cells, which suggests that vonoprazan might be an alternative to PPIs, with no interference with the therapeutic effects of anti-VEGF cancer chemotherapy.","ja":"Proton pump inhibitors (PPIs) are potent inhibitors of gastric acid secretion, used as first-line agents in treating peptic ulcers. However, we have previously reported that PPIs may diminish the therapeutic effect of anti-vascular endothelial growth factor (VEGF) drugs in patients with cancer. In this study, we explored the effects of vonoprazan, a novel gastric acid secretion inhibitor used for the treatment of peptic ulcers, on the secretion of VEGF in cancer cells and attempted to propose it as an alternative PPI for cancer chemotherapy. The effects of PPI and vonoprazan on VEGF expression in cancer cells were compared by real-time reverse transcription-polymerase chain reaction and ELISA. The interaction of vonoprazan and PPIs with transcriptional regulators by docking simulation analysis. In various cancer cell lines, including the human colorectal cancer cell line (LS174T), PPI increased VEGF messenger RNA expression and VEGF protein secretion, while this effect was not observed with vonoprazan. Molecular docking simulation analysis showed that vonoprazan had a lower binding affinity for estrogen receptor alpha (ER-α), one of the transcriptional regulators of VEGF, compared to PPI. Although the PPI-induced increase in VEGF expression was counteracted by pharmacological ER-α inhibition, the effect of vonoprazan on VEGF expression was unchanged. Vonoprazan does not affect VEGF expression in cancer cells, which suggests that vonoprazan might be an alternative to PPIs, with no interference with the therapeutic effects of anti-VEGF cancer chemotherapy."},"publication_date":"2022-12-09","publication_name":{"en":"Drug Development Research","ja":"Drug Development Research"},"volume":"Vol.84","number":"No.1","starting_page":"75","ending_page":"83","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1002/ddr.22013"],"issn":["1098-2299"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:12, {"insert":{"user_id":"B000337971","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/36169161","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=394582","label":"url"}],"paper_title":{"en":"Non-recovery of vancomycin-associated nephrotoxicity is related to worsening survival outcomes: Combined retrospective analyses of two real-world databases.","ja":"Non-recovery of vancomycin-associated nephrotoxicity is related to worsening survival outcomes: Combined retrospective analyses of two real-world databases."},"authors":{"en":[{"name":"Chuma Masayuki"},{"name":"Hamano Hirofumi"},{"name":"Bando Takashi"},{"name":"Kondo Masateru"},{"name":"Okada Naoto"},{"name":"Izumi Yuki"},{"name":"Ishida Shunsuke"},{"name":"Yoshioka Toshihiko"},{"name":"Asada Mizuho"},{"name":"Niimura Takahiro"},{"name":"Zamami Yoshito"},{"name":"Takechi Kenshi"},{"name":"Goda Mitsuhiro"},{"name":"Miyata Koji"},{"name":"Yagi Kenta"},{"name":"Kasamo Sachiko"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Azuma Momoyo"},{"name":"Yanagawa Hiroaki"},{"name":"Tasaki Yoshikazu"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"中馬 真幸"},{"name":"濱野 裕章"},{"name":"Bando Takashi"},{"name":"Kondo Masateru"},{"name":"岡田 直人"},{"name":"Izumi Yuki"},{"name":"Ishida Shunsuke"},{"name":"Yoshioka Toshihiko"},{"name":"Asada Mizuho"},{"name":"新村 貴博"},{"name":"座間味 義人"},{"name":"武智 研志"},{"name":"合田 光寛"},{"name":"Miyata Koji"},{"name":"八木 健太"},{"name":"Kasamo Sachiko"},{"name":"石澤 有紀"},{"name":"東 桃代"},{"name":"楊河 宏章"},{"name":"Tasaki Yoshikazu"},{"name":"石澤 啓介"}]},"description":{"en":"There has been growing concern in worsening survival and renal outcomes following vancomycin-associated nephrotoxicity (VAN) onset, but the factors associated with these phenomena remain unclear. To examine these factors, we performed a retrospective study combining the analysis of two real-world databases. Initially, the FDA Adverse Event Reporting System (FAERS) was used to evaluate the relationship between VAN and mortality using odds ratios (ORs) and 95% confidence intervals (CIs). Next, electronic medical records (EMRs) were examined in a more robust cohort for evaluation of the association between renal outcomes and worsening survival using Cox proportional hazards regression models. FAERS analysis revealed a significant correlation between VAN occurrence and increased mortality (OR: 1.30; 95% CI: 1.17-1.46). EMR analysis showed that non-recovery of VAN was associated with increased hospital mortality (hazard ratio [HR]: 4.05; 95% CI: 2.42-6.77) and 1-year mortality (HR: 3.03, 95% CI: 1.98-4.64). The HR for VAN recovery was lower for patients with acute kidney injury (AKI) stage 2 (HR: 0.09; 95% CI: 0.02-0.40). Thus, worsening survival outcomes were associated with non-recovery of VAN, whereby AKI stage 2 was a significant risk factor. Progression to severe VAN should be prevented for better survival outcomes.","ja":"There has been growing concern in worsening survival and renal outcomes following vancomycin-associated nephrotoxicity (VAN) onset, but the factors associated with these phenomena remain unclear. To examine these factors, we performed a retrospective study combining the analysis of two real-world databases. Initially, the FDA Adverse Event Reporting System (FAERS) was used to evaluate the relationship between VAN and mortality using odds ratios (ORs) and 95% confidence intervals (CIs). Next, electronic medical records (EMRs) were examined in a more robust cohort for evaluation of the association between renal outcomes and worsening survival using Cox proportional hazards regression models. FAERS analysis revealed a significant correlation between VAN occurrence and increased mortality (OR: 1.30; 95% CI: 1.17-1.46). EMR analysis showed that non-recovery of VAN was associated with increased hospital mortality (hazard ratio [HR]: 4.05; 95% CI: 2.42-6.77) and 1-year mortality (HR: 3.03, 95% CI: 1.98-4.64). The HR for VAN recovery was lower for patients with acute kidney injury (AKI) stage 2 (HR: 0.09; 95% CI: 0.02-0.40). Thus, worsening survival outcomes were associated with non-recovery of VAN, whereby AKI stage 2 was a significant risk factor. Progression to severe VAN should be prevented for better survival outcomes."},"publication_date":"2022-10-07","publication_name":{"en":"Basic & Clinical Pharmacology & Toxicology","ja":"Basic & Clinical Pharmacology & Toxicology"},"volume":"Vol.131","number":"No.6","starting_page":"525","ending_page":"535","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1111/bcpt.13799"],"issn":["1742-7843"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:13, {"insert":{"user_id":"B000337971","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/117365","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/35659512","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=390279","label":"url"}],"paper_title":{"en":"Investigation of drugs for the prevention of doxorubicin-induced cardiac events using big data analysis.","ja":"Investigation of drugs for the prevention of doxorubicin-induced cardiac events using big data analysis."},"authors":{"en":[{"name":"Nishiuchi Shiori"},{"name":"Yagi Kenta"},{"name":"Saito Hiroumi"},{"name":"Zamami Yoshito"},{"name":"Niimura Takahiro"},{"name":"Miyata Koji"},{"name":"Sakamoto Yoshika"},{"name":"Fukunaga Kimiko"},{"name":"Ishida Shunsuke"},{"name":"Hamano Hirofumi"},{"name":"Aizawa Fuka"},{"name":"Goda Mitsuhiro"},{"name":"Chuma Masayuki"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Nawa Hideki"},{"name":"Yanagawa Hiroaki"},{"name":"Kanda Yasunari"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"西内 栞"},{"name":"八木 健太"},{"name":"齊藤 広海"},{"name":"座間味 義人"},{"name":"新村 貴博"},{"name":"宮田 晃志"},{"name":"阪本 淑華"},{"name":"Fukunaga Kimiko"},{"name":"Ishida Shunsuke"},{"name":"濱野 裕章"},{"name":"相澤 風花"},{"name":"合田 光寛"},{"name":"中馬 真幸"},{"name":"石澤 有紀"},{"name":"Nawa Hideki"},{"name":"楊河 宏章"},{"name":"Kanda Yasunari"},{"name":"石澤 啓介"}]},"description":{"en":"These findings suggest that doxorubicin-induced cardiac events are suppressed by the administration of mosapride and sirolimus.","ja":"The Gene Expression Omnibus (GEO), Library of Integrated Network-based Cellular Signatures (LINCS), and Food and Drug Administration Adverse Events Reporting System (FAERS) databases were used to extract candidate prophylactic drugs. Mouse models of doxorubicin-induced cardiac events were generated by intraperitoneal administration of 20 mg/kg of doxorubicin on Day 1 and oral administration of prophylactic candidate drugs for 6 consecutive days beginning the day before doxorubicin administration. On Day 6, mouse hearts were extracted and examined for mRNA expression of apoptosis-related genes."},"publication_date":"2022-05","publication_name":{"en":"European Journal of Pharmacology","ja":"European Journal of Pharmacology"},"volume":"Vol.928","number":"No.175083","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1016/j.ejphar.2022.175083"],"issn":["1879-0712"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:14, {"insert":{"user_id":"B000337971","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/117366","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/35445533","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=390280","label":"url"}],"paper_title":{"en":"Discovery of preventive drugs for cisplatin-induced acute kidney injury using big data analysis.","ja":"Discovery of preventive drugs for cisplatin-induced acute kidney injury using big data analysis."},"authors":{"en":[{"name":"Kanda Masaya"},{"name":"Goda Mitsuhiro"},{"name":"Maegawa Akiko"},{"name":"Yoshioka Toshihiko"},{"name":"Yoshida Ami"},{"name":"Miyata Koji"},{"name":"Aizawa Fuka"},{"name":"Niimura Takahiro"},{"name":"Hamano Hirofumi"},{"name":"Okada Naoto"},{"name":"Sakurada Takumi"},{"name":"Chuma Masayuki"},{"name":"Yagi Kenta"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Yanagawa Hiroaki"},{"name":"Zamami Yoshito"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"Kanda Masaya"},{"name":"合田 光寛"},{"name":"Maegawa Akiko"},{"name":"Yoshioka Toshihiko"},{"name":"Yoshida Ami"},{"name":"Miyata Koji"},{"name":"相澤 風花"},{"name":"新村 貴博"},{"name":"濱野 裕章"},{"name":"岡田 直人"},{"name":"Sakurada Takumi"},{"name":"中馬 真幸"},{"name":"八木 健太"},{"name":"石澤 有紀"},{"name":"楊河 宏章"},{"name":"座間味 義人"},{"name":"石澤 啓介"}]},"description":{"en":"Cisplatin is effective against many types of carcinoma. However, a high rate of renal damage is a clinical problem. Thus, there is a need to establish a method to prevent it. Although various compounds have been reported to be effective against cisplatin-induced renal injury, there are no examples of their clinical application. Therefore, we attempted to search for prophylactic agents with a high potential for clinical application. We used Cascade Eye to identify genes that are altered during cisplatin-induced renal injury, Library of Integrated Network-based Cellular Signatures (LINCS) to identify drugs that inhibit changes in gene expression, and a large database of spontaneous adverse drug reaction reports to identify drugs that could prevent cisplatin-induced kidney injury in clinical practice. In total, 10 candidate drugs were identified. Using the US Food and Drug Administration (FDA) Adverse Event Reporting System (FAERS), we identified drugs that reduce cisplatin-induced kidney injury. Fenofibrate was selected as a candidate drug to prevent cisplatin-induced kidney injury based on the FAERS analysis. A model was used to evaluate the efficacy of fenofibrate against cisplatin-induced renal injury. Studies using HK2 cells and mouse models showed that fenofibrate significantly inhibited cisplatin-induced renal injury but did not inhibit the antitumor effect of cisplatin. Fenofibrate is a candidate prophylactic drug with high clinical applicability for cisplatin-induced renal injury. Analysis of data from multiple big databases will improve the search for novel prophylactic drugs with high clinical applicability. For the practical application of these findings, evaluation in prospective controlled trials is necessary.","ja":"Cisplatin is effective against many types of carcinoma. However, a high rate of renal damage is a clinical problem. Thus, there is a need to establish a method to prevent it. Although various compounds have been reported to be effective against cisplatin-induced renal injury, there are no examples of their clinical application. Therefore, we attempted to search for prophylactic agents with a high potential for clinical application. We used Cascade Eye to identify genes that are altered during cisplatin-induced renal injury, Library of Integrated Network-based Cellular Signatures (LINCS) to identify drugs that inhibit changes in gene expression, and a large database of spontaneous adverse drug reaction reports to identify drugs that could prevent cisplatin-induced kidney injury in clinical practice. In total, 10 candidate drugs were identified. Using the US Food and Drug Administration (FDA) Adverse Event Reporting System (FAERS), we identified drugs that reduce cisplatin-induced kidney injury. Fenofibrate was selected as a candidate drug to prevent cisplatin-induced kidney injury based on the FAERS analysis. A model was used to evaluate the efficacy of fenofibrate against cisplatin-induced renal injury. Studies using HK2 cells and mouse models showed that fenofibrate significantly inhibited cisplatin-induced renal injury but did not inhibit the antitumor effect of cisplatin. Fenofibrate is a candidate prophylactic drug with high clinical applicability for cisplatin-induced renal injury. Analysis of data from multiple big databases will improve the search for novel prophylactic drugs with high clinical applicability. For the practical application of these findings, evaluation in prospective controlled trials is necessary."},"publication_date":"2022-04-30","publication_name":{"en":"Clinical and Translational Science","ja":"Clinical and Translational Science"},"volume":"Vol.15","number":"No.7","starting_page":"1664","ending_page":"1675","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1111/cts.13282"],"issn":["1752-8062"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:15, {"insert":{"user_id":"B000337971","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/35464114","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=390276","label":"url"}],"paper_title":{"en":"A web-based survey of educational opportunities of medical professionals based on changes in conference design during the COVID-19 pandemic.","ja":"A web-based survey of educational opportunities of medical professionals based on changes in conference design during the COVID-19 pandemic."},"authors":{"en":[{"name":"Yagi Kenta"},{"name":"Sato Yasutaka"},{"name":"Sakaguchi Satoshi"},{"name":"Goda Mitsuhiro"},{"name":"Hamano Hirofumi"},{"name":"Aizawa Fuka"},{"name":"Shimizu Mayuko"},{"name":"Inoue-Hamano Arisa"},{"name":"Nishimori Toshihide"},{"name":"Tagi Masato"},{"name":"Kanno Marina"},{"name":"Matsuoka-Ando Rie"},{"name":"Yoshioka Toshihiko"},{"name":"Matstubara Yoshiko"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Shimizu Rieko"},{"name":"Maruo Akinori"},{"name":"Kuniki Yurika"},{"name":"Sakamoto Yoshika"},{"name":"Itobayashi Sayuri"},{"name":"Zamami Yoshito"},{"name":"Yanagawa Hiroaki"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"八木 健太"},{"name":"Sato Yasutaka"},{"name":"坂口 暁"},{"name":"合田 光寛"},{"name":"濱野 裕章"},{"name":"相澤 風花"},{"name":"清水 真祐子"},{"name":"Inoue-Hamano Arisa"},{"name":"Nishimori Toshihide"},{"name":"田木 真和"},{"name":"Kanno Marina"},{"name":"Matsuoka-Ando Rie"},{"name":"吉岡 俊彦"},{"name":"Matstubara Yoshiko"},{"name":"石澤 有紀"},{"name":"Shimizu Rieko"},{"name":"Maruo Akinori"},{"name":"國木 悠理香"},{"name":"阪本 淑華"},{"name":"糸林 小友理"},{"name":"座間味 義人"},{"name":"楊河 宏章"},{"name":"石澤 啓介"}]},"description":{"en":"The online version contains supplementary material available at 10.1007/s10639-022-11032-5.","ja":"The online version contains supplementary material available at 10.1007/s10639-022-11032-5."},"publication_date":"2022-04-18","publication_name":{"en":"Education and Information Technologies","ja":"Education and Information Technologies"},"volume":"Vol.27","starting_page":"10371","ending_page":"10386","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1007/s10639-022-11032-5"],"issn":["1360-2357"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:16, {"insert":{"user_id":"B000337971","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/117810","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/35262686","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=390814","label":"url"}],"paper_title":{"en":"Association between statin use and daptomycin-related musculoskeletal adverse events: A mixed approach combining a meta-analysis and a disproportionality analysis.","ja":"Association between statin use and daptomycin-related musculoskeletal adverse events: A mixed approach combining a meta-analysis and a disproportionality analysis."},"authors":{"en":[{"name":"Chuma Masayuki"},{"name":"Nakamoto Aki"},{"name":"Bando Takashi"},{"name":"Niimura Takahiro"},{"name":"Kondo Yutaka"},{"name":"Hamano Hirofumi"},{"name":"Okada Naoto"},{"name":"Asada Mizuho"},{"name":"Zamami Yoshito"},{"name":"Takechi Kenshi"},{"name":"Goda Mitsuhiro"},{"name":"Miyata Koji"},{"name":"Yagi Kenta"},{"name":"Yoshioka Toshihiko"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Yanagawa Hiroaki"},{"name":"Tasaki Yoshikazu"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"中馬 真幸"},{"name":"中本 亜樹"},{"name":"坂東 貴司"},{"name":"新村 貴博"},{"name":"Kondo Yutaka"},{"name":"濱野 裕章"},{"name":"岡田 直人"},{"name":"Asada Mizuho"},{"name":"座間味 義人"},{"name":"武智 研志"},{"name":"合田 光寛"},{"name":"宮田 晃志"},{"name":"八木 健太"},{"name":"吉岡 俊彦"},{"name":"石澤 有紀"},{"name":"楊河 宏章"},{"name":"Tasaki Yoshikazu"},{"name":"石澤 啓介"}]},"description":{"en":"There is a growing concern about the association between the combined use of daptomycin (DAP) and statins and the occurrence of musculoskeletal adverse events (MAEs), but this remains controversial. This study aimed to clarify the association between statin use and DAP-related MAEs. We used a mixed approach that combines two methodologies. First, we conducted a meta-analysis to examine the effects of statin use on DAP-related MAEs. Second, we conducted a disproportionality analysis using the FDA Adverse Events Reporting System (FAERS) to further confirm the results of the meta-analysis and to examine the effect of each type of statin on DAP-related MAEs in a large population. In the meta-analysis, statin use significantly increased the incidence of DAP-related rhabdomyolysis (odds ratio [OR]: 3.83, 95% confidence interval [CI]: 1.43-10.26) but not DAP-related myopathy (OR: 1.72, 95% CI: 0.95-3.12). In the disproportionality analysis using the FAERS, the use of statin significantly increased the reporting OR (ROR) for DAP-related myopathy (ROR: 5.69, 95% CI: 4.31-7.51) and rhabdomyolysis (ROR: 5.77, 95% CI: 4.33-7.68). Atorvastatin, rosuvastatin, and simvastatin all increased the incidence of DAP-related myopathy and rhabdomyolysis. The mixed approach combining a meta-analysis and disproportionality analysis showed that statin use was associated with the occurrence of DAP-related rhabdomyolysis. The appropriate use of statins and DAP should be performed with careful consideration of its safety.","ja":"There is a growing concern about the association between the combined use of daptomycin (DAP) and statins and the occurrence of musculoskeletal adverse events (MAEs), but this remains controversial. This study aimed to clarify the association between statin use and DAP-related MAEs. We used a mixed approach that combines two methodologies. First, we conducted a meta-analysis to examine the effects of statin use on DAP-related MAEs. Second, we conducted a disproportionality analysis using the FDA Adverse Events Reporting System (FAERS) to further confirm the results of the meta-analysis and to examine the effect of each type of statin on DAP-related MAEs in a large population. In the meta-analysis, statin use significantly increased the incidence of DAP-related rhabdomyolysis (odds ratio [OR]: 3.83, 95% confidence interval [CI]: 1.43-10.26) but not DAP-related myopathy (OR: 1.72, 95% CI: 0.95-3.12). In the disproportionality analysis using the FAERS, the use of statin significantly increased the reporting OR (ROR) for DAP-related myopathy (ROR: 5.69, 95% CI: 4.31-7.51) and rhabdomyolysis (ROR: 5.77, 95% CI: 4.33-7.68). Atorvastatin, rosuvastatin, and simvastatin all increased the incidence of DAP-related myopathy and rhabdomyolysis. The mixed approach combining a meta-analysis and disproportionality analysis showed that statin use was associated with the occurrence of DAP-related rhabdomyolysis. The appropriate use of statins and DAP should be performed with careful consideration of its safety."},"publication_date":"2022-03-09","publication_name":{"en":"Clinical Infectious Diseases","ja":"Clinical Infectious Diseases"},"volume":"Vol.75","number":"No.8","starting_page":"1416","ending_page":"1422","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1093/cid/ciac128"],"issn":["1537-6591"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:17, {"insert":{"user_id":"B000337971","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/117414","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/35240525","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=388515","label":"url"}],"paper_title":{"en":"Identification of prophylactic drugs for oxaliplatin-induced peripheral neuropathy using big data.","ja":"Identification of prophylactic drugs for oxaliplatin-induced peripheral neuropathy using big data."},"authors":{"en":[{"name":"Zamami Yoshito"},{"name":"Niimura Takahiro"},{"name":"Kawashiri Takehiro"},{"name":"Goda Mitsuhiro"},{"name":"Naito Yutaro"},{"name":"Fukushima Keijo"},{"name":"Ushio Soichiro"},{"name":"Aizawa Fuka"},{"name":"Hamano Hirofumi"},{"name":"Okada Naoto"},{"name":"Yagi Kenta"},{"name":"Miyata Koji"},{"name":"Takechi Kenshi"},{"name":"Chuma Masayuki"},{"name":"Koyama Toshihiro"},{"name":"Kobayashi Daisuke"},{"name":"Shimazoe Takao"},{"name":"Fujino Hiromichi"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"座間味 義人"},{"name":"新村 貴博"},{"name":"Kawashiri Takehiro"},{"name":"合田 光寛"},{"name":"Naito Yutaro"},{"name":"福島 圭穣"},{"name":"Ushio Soichiro"},{"name":"相澤 風花"},{"name":"濱野 裕章"},{"name":"岡田 直人"},{"name":"八木 健太"},{"name":"Miyata Koji"},{"name":"武智 研志"},{"name":"中馬 真幸"},{"name":"Koyama Toshihiro"},{"name":"Kobayashi Daisuke"},{"name":"Shimazoe Takao"},{"name":"藤野 裕道"},{"name":"石澤 有紀"},{"name":"石澤 啓介"}]},"description":{"en":"Thus, drug repositioning using data from large-scale basic and clinical databases enables the discovery of new indications for approved drugs with a high probability of success.","ja":"Thus, drug repositioning using data from large-scale basic and clinical databases enables the discovery of new indications for approved drugs with a high probability of success."},"publication_date":"2022-02-28","publication_name":{"en":"Biomedicine & Pharmacotherapy","ja":"Biomedicine & Pharmacotherapy"},"volume":"Vol.148","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1016/j.biopha.2022.112744"],"issn":["1950-6007"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:18, {"insert":{"user_id":"B000337971","type":"published_papers","id":"32553179"},"force":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/116008","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/33982438","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=375733","label":"url"}],"paper_title":{"en":"Effects of 5-HT3 receptor antagonists on cisplatin-induced kidney injury.","ja":"Effects of 5-HT3 receptor antagonists on cisplatin-induced kidney injury."},"authors":{"en":[{"name":"Goda Mitsuhiro"},{"name":"Kanda Masaya"},{"name":"Yoshioka Toshihiko"},{"name":"Yoshida Ami"},{"name":"Murai Yoichi"},{"name":"Zamami Yoshito"},{"name":"Aizawa Fuka"},{"name":"Niimura Takahiro"},{"name":"Hamano Hirofumi"},{"name":"Okada Naoto"},{"name":"Yagi Kenta"},{"name":"Chuma Masayuki"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"合田 光寛"},{"name":"Kanda Masaya"},{"name":"Yoshioka Toshihiko"},{"name":"Yoshida Ami"},{"name":"Murai Yoichi"},{"name":"座間味 義人"},{"name":"相澤 風花"},{"name":"新村 貴博"},{"name":"濱野 裕章"},{"name":"岡田 直人"},{"name":"八木 健太"},{"name":"中馬 真幸"},{"name":"石澤 有紀"},{"name":"石澤 啓介"}]},"description":{"en":"receptor antagonists do not worsen cisplatin-induced acute kidney injury. The findings should be validated in a prospective controlled trial before implementation in clinical practice.","ja":"receptor antagonists do not worsen cisplatin-induced acute kidney injury. The findings should be validated in a prospective controlled trial before implementation in clinical practice."},"publication_date":"2021-05-13","publication_name":{"en":"Clinical and Translational Science","ja":"Clinical and Translational Science"},"languages":["eng"],"referee":true,"identifiers":{"doi":["10.1111/cts.13045"],"issn":["1752-8062"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:19, {"insert":{"user_id":"B000337971","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"http://repo.lib.tokushima-u.ac.jp/116038","label":"url"},{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/116038","label":"url"},{"@id":"https://cir.nii.ac.jp/crid/1050851320431028352/","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=390121","label":"url"}],"paper_title":{"en":"薬剤誘発性大動脈解離易発症モデルマウスを用いた薬効評価","ja":"薬剤誘発性大動脈解離易発症モデルマウスを用いた薬効評価"},"authors":{"en":[{"name":"Izawa-Ishizawa Yuki"},{"name":"Goda Mitsuhiro"},{"name":"Aizawa Fuka"},{"name":"Zamami Yoshito"},{"name":"Hamano Hirofumi"},{"name":"Yagi Kenta"},{"name":"Ikeda Yasumasa"},{"name":"Ishizawa Keisuke"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"石澤 有紀"},{"name":"合田 光寛"},{"name":"相澤 風花"},{"name":"座間味 義人"},{"name":"濱野 裕章"},{"name":"八木 健太"},{"name":"池田 康将"},{"name":"石澤 啓介"},{"name":"玉置 俊晃"}]},"description":{"en":"Aortic dissection (or dissecting aortic aneurysm) is a condition in which the aortic wall is separated into two layers at the medial level to form a pseudocavity. The intima crack, called the ``entry'', allows blood to tear through the medial layer and flow in. The location of the ``entry'' and the extent of the dissection can cause a variety of serious complications, including rupture, cardiac tamponade, and obstruction of branched vessels. According to the Guideline on Diagnosis and Treatment of Aortic Aneurysm and Aortic Dissection 2020, it is estimated that 61.4% of the onset of dissection die before arrival at the hospital, and 93% will die within 24 hours after the onset. It has been suggested that the morbidity rate has been increasing in recent years. Since many of them have a fatal prognosis, it is an important issue to prevent the onset itself. However, no effective therapeutic agent or preventive strategy has been established so far. The first reason is that it is extremely difficult to design clinical studies because aortic dissection traced the rapid onset and progression. The second is that the pathophysiology and preventive drug search are not sufficiently conducted even at the basic research level. Epidemiologically, the results of the International Registry of Aortic Dissection (IRAD) revealed that aging, hypertension, atherosclerosis, and hereditary connective tissue diseases are risk factors. The aortic aneurysm also shows similar pathological conditions caused by these risk factors. However, one of the major differences between aneurysm and dissection is the presence of aortic intima rupture. Therefore, we attempted to establish a mouse model developing dissection at a high rate by adding the endothelial dysfunction to a pharmacologically induced aortic aneurysm model mouse. Furthermore, we evaluated the efficacy of pitavastatin and several nutrients using our novel model mice and verified its usefulness as a model animal.","ja":"Aortic dissection (or dissecting aortic aneurysm) is a condition in which the aortic wall is separated into two layers at the medial level to form a pseudocavity. The intima crack, called the ``entry'', allows blood to tear through the medial layer and flow in. The location of the ``entry'' and the extent of the dissection can cause a variety of serious complications, including rupture, cardiac tamponade, and obstruction of branched vessels. According to the Guideline on Diagnosis and Treatment of Aortic Aneurysm and Aortic Dissection 2020, it is estimated that 61.4% of the onset of dissection die before arrival at the hospital, and 93% will die within 24 hours after the onset. It has been suggested that the morbidity rate has been increasing in recent years. Since many of them have a fatal prognosis, it is an important issue to prevent the onset itself. However, no effective therapeutic agent or preventive strategy has been established so far. The first reason is that it is extremely difficult to design clinical studies because aortic dissection traced the rapid onset and progression. The second is that the pathophysiology and preventive drug search are not sufficiently conducted even at the basic research level. Epidemiologically, the results of the International Registry of Aortic Dissection (IRAD) revealed that aging, hypertension, atherosclerosis, and hereditary connective tissue diseases are risk factors. The aortic aneurysm also shows similar pathological conditions caused by these risk factors. However, one of the major differences between aneurysm and dissection is the presence of aortic intima rupture. Therefore, we attempted to establish a mouse model developing dissection at a high rate by adding the endothelial dysfunction to a pharmacologically induced aortic aneurysm model mouse. Furthermore, we evaluated the efficacy of pitavastatin and several nutrients using our novel model mice and verified its usefulness as a model animal."},"publication_date":"2021-04-25","publication_name":{"en":"Shikoku Acta Medica","ja":"四国医学雑誌"},"volume":"Vol.77","number":"No.1,2","starting_page":"57","ending_page":"62","languages":["jpn"],"referee":true,"identifiers":{"issn":["0037-3699"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:20, {"insert":{"user_id":"B000337971","type":"published_papers","id":"32553180"},"force":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/116301","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/33910036","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=375760","label":"url"}],"paper_title":{"en":"Examination of the antiepileptic effects of valacyclovir using kindling mice- search for novel antiepileptic agents by drug repositioning using a large medical information database.","ja":"Examination of the antiepileptic effects of valacyclovir using kindling mice- search for novel antiepileptic agents by drug repositioning using a large medical information database."},"authors":{"en":[{"name":"Takahashi Shimon"},{"name":"Takechi Kenshi"},{"name":"Jozukuri Natsumi"},{"name":"Niimura Takahiro"},{"name":"Chuma Masayuki"},{"name":"Goda Mitsuhiro"},{"name":"Zamami Yoshito"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Imanishi Masaki"},{"name":"Horinouchi Yuya"},{"name":"Ikeda Yasumasa"},{"name":"Tsuchiya Koichiro"},{"name":"Yanagawa Hiroaki"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"Takahashi Shimon"},{"name":"武智 研志"},{"name":"Jozukuri Natsumi"},{"name":"新村 貴博"},{"name":"中馬 真幸"},{"name":"合田 光寛"},{"name":"座間味 義人"},{"name":"石澤 有紀"},{"name":"今西 正樹"},{"name":"堀ノ内 裕也"},{"name":"池田 康将"},{"name":"土屋 浩一郎"},{"name":"楊河 宏章"},{"name":"石澤 啓介"}]},"description":{"en":"Despite the availability of more than 20 clinical antiepileptic drugs, approximately 30% of patients with epilepsy do not respond to antiepileptic drug treatment. Therefore, it is important to develop antiepileptic products that function via novel mechanisms. In the present study, we evaluated data from one of the largest global databases to identify drugs with antiepileptic effects, and subsequently attempted to understand the effect of the combination of antiepileptic drugs and valacyclovir in epileptic seizures using a kindling model. To induce kindling in mice, pentylenetetrazol at a dose of 40 mg/kg was administered once every 48 h. Valacyclovir was orally administered 30 min before antiepileptic drug injection in kindled mice, and behavioral seizures were monitored for 20 min following pentylenetetrazol administration. Additionally, c-Fos expression in the hippocampal dentate gyrus was measured in kindled mice. Valacyclovir showed inhibitory effects on pentylenetetrazol-induced kindled seizures. In addition, simultaneous use of levetiracetam and valacyclovir caused more potent inhibition of seizure activity, and neither valproic acid nor diazepam augmented the anti-seizure effect in kindled mice. Furthermore, kindled mice showed increased c-Fos levels in the dentate gyrus. The increase in c-Fos expression was significantly inhibited by the simultaneous use of levetiracetam and valacyclovir. The findings of the present study indicate that a combination of levetiracetam and valacyclovir had possible anticonvulsive effects on pentylenetetrazol-induced kindled epileptic seizures. These results suggest that valacyclovir may have an antiseizure effect in patients with epilepsy.","ja":"Despite the availability of more than 20 clinical antiepileptic drugs, approximately 30% of patients with epilepsy do not respond to antiepileptic drug treatment. Therefore, it is important to develop antiepileptic products that function via novel mechanisms. In the present study, we evaluated data from one of the largest global databases to identify drugs with antiepileptic effects, and subsequently attempted to understand the effect of the combination of antiepileptic drugs and valacyclovir in epileptic seizures using a kindling model. To induce kindling in mice, pentylenetetrazol at a dose of 40 mg/kg was administered once every 48 h. Valacyclovir was orally administered 30 min before antiepileptic drug injection in kindled mice, and behavioral seizures were monitored for 20 min following pentylenetetrazol administration. Additionally, c-Fos expression in the hippocampal dentate gyrus was measured in kindled mice. Valacyclovir showed inhibitory effects on pentylenetetrazol-induced kindled seizures. In addition, simultaneous use of levetiracetam and valacyclovir caused more potent inhibition of seizure activity, and neither valproic acid nor diazepam augmented the anti-seizure effect in kindled mice. Furthermore, kindled mice showed increased c-Fos levels in the dentate gyrus. The increase in c-Fos expression was significantly inhibited by the simultaneous use of levetiracetam and valacyclovir. The findings of the present study indicate that a combination of levetiracetam and valacyclovir had possible anticonvulsive effects on pentylenetetrazol-induced kindled epileptic seizures. These results suggest that valacyclovir may have an antiseizure effect in patients with epilepsy."},"publication_date":"2021-04-25","publication_name":{"en":"European Journal of Pharmacology","ja":"European Journal of Pharmacology"},"volume":"Vol.902","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1016/j.ejphar.2021.174099"],"issn":["1879-0712"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:21, {"insert":{"user_id":"B000337971","type":"published_papers","id":"31136394"},"force":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/116288","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/33231381","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=372620","label":"url"}],"paper_title":{"en":"Investigation of drugs affecting hypertension in bevacizumab-treated patients and examination of the impact on the therapeutic effect.","ja":"Investigation of drugs affecting hypertension in bevacizumab-treated patients and examination of the impact on the therapeutic effect."},"authors":{"en":[{"name":"Yagi Kenta"},{"name":"Mitstui Marin"},{"name":"Zamami Yoshito"},{"name":"Niimura Takahiro"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Goda Mitsuhiro"},{"name":"Chuma Masayuki"},{"name":"Fukunaga Kimiko"},{"name":"Shibata Takahiro"},{"name":"Ishida Shunsuke"},{"name":"Sakurada Takumi"},{"name":"Okada Naoto"},{"name":"Hamano Hirofumi"},{"name":"Horinouchi Yuya"},{"name":"Ikeda Yasumasa"},{"name":"Yanagawa Hiroaki"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"八木 健太"},{"name":"Mitstui Marin"},{"name":"座間味 義人"},{"name":"新村 貴博"},{"name":"石澤 有紀"},{"name":"合田 光寛"},{"name":"中馬 真幸"},{"name":"Fukunaga Kimiko"},{"name":"Shibata Takahiro"},{"name":"Ishida Shunsuke"},{"name":"Sakurada Takumi"},{"name":"岡田 直人"},{"name":"Hamano Hirofumi"},{"name":"堀ノ内 裕也"},{"name":"池田 康将"},{"name":"楊河 宏章"},{"name":"石澤 啓介"}]},"description":{"en":"PPIs prevent hypertension in bevacizumab-treated patients but may reduce bevacizumab's anti-tumoral effects by inducing VEGF expression.","ja":"PPIs prevent hypertension in bevacizumab-treated patients but may reduce bevacizumab's anti-tumoral effects by inducing VEGF expression."},"publication_date":"2020-11-24","publication_name":{"en":"Cancer Medicine","ja":"Cancer Medicine"},"languages":["eng"],"referee":true,"identifiers":{"doi":["10.1002/cam4.3587"],"issn":["2045-7634"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:22, {"insert":{"user_id":"B000337971","type":"published_papers","id":"30377885"},"force":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/115332","label":"url"},{"@id":"https://www.scopus.com/record/display.url?eid=2-s2.0-85091999803&origin=inward","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=371707","label":"url"}],"paper_title":{"en":"Preventive Effects of Quercetin against the Onset of Atherosclerosis-Related Acute Aortic Syndromes in Mice","ja":"Preventive Effects of Quercetin against the Onset of Atherosclerosis-Related Acute Aortic Syndromes in Mice"},"authors":{"en":[{"name":"Masateru Kondo"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Goda Mitsuhiro"},{"name":"Mayuko Hosooka"},{"name":"Yuu Kagimoto"},{"name":"Naoko Saito"},{"name":"Rie Matsuoka"},{"name":"Zamami Yoshito"},{"name":"Chuma Masayuki"},{"name":"Yagi Kenta"},{"name":"Takechi Kenshi"},{"name":"Tsuneyama Koichi"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"近藤 正輝"},{"name":"石澤 有紀"},{"name":"合田 光寛"},{"name":"細岡 真由子"},{"name":"鍵本 優有"},{"name":"齋藤 尚子"},{"name":"松岡 里英"},{"name":"座間味 義人"},{"name":"中馬 真幸"},{"name":"八木 健太"},{"name":"武智 研志"},{"name":"常山 幸一"},{"name":"石澤 啓介"}]},"publication_date":"2020-09-30","publication_name":{"en":"International Journal of Molecular Sciences","ja":"International Journal of Molecular Sciences"},"volume":"Vol.21","number":"No.19","languages":["eng"],"referee":true,"identifiers":{"doi":["10.3390/ijms21197226"],"issn":["1422-0067"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:23, {"insert":{"user_id":"B000337971","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/114409","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/32430665","label":"url"},{"@id":"https://www.scopus.com/record/display.url?eid=2-s2.0-85085484596&origin=inward","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=363775","label":"url"}],"paper_title":{"en":"Deletion of H-ferritin in macrophages alleviates obesity and diabetes induced by high-fat diet in mice","ja":"Deletion of H-ferritin in macrophages alleviates obesity and diabetes induced by high-fat diet in mice"},"authors":{"en":[{"name":"Ikeda Yasumasa"},{"name":"Watanabe Hiroaki"},{"name":"Shiuchi Tetsuya"},{"name":"Hamano Hirofumi"},{"name":"Horinouchi Yuya"},{"name":"Imanishi Masaki"},{"name":"Goda Mitsuhiro"},{"name":"Zamami Yoshito"},{"name":"Takechi Kenshi"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Miyamoto Licht"},{"name":"Ishizawa Keisuke"},{"name":"Aihara Ken-ichi"},{"name":"Tsuchiya Koichiro"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"池田 康将"},{"name":"渡邊 大晃"},{"name":"志内 哲也"},{"name":"濱野 裕章"},{"name":"堀ノ内 裕也"},{"name":"今西 正樹"},{"name":"合田 光寛"},{"name":"座間味 義人"},{"name":"武智 研志"},{"name":"石澤 有紀"},{"name":"宮本 理人"},{"name":"石澤 啓介"},{"name":"粟飯原 賢一"},{"name":"土屋 浩一郎"},{"name":"玉置 俊晃"}]},"description":{"en":"Iron accumulation affects obesity and diabetes, both of which are ameliorated by iron reduction. Ferritin, an iron-storage protein, plays a crucial role in iron metabolism. H-ferritin exerts its cytoprotective action by reducing toxicity via its ferroxidase activity. We investigated the role of macrophage H-ferritin in obesity and diabetes. Conditional macrophage-specific H-ferritin (Fth, also known as Fth1) knockout (LysM-Cre Fth KO) mice were used and divided into four groups: wild-type (WT) and LysM-Cre Fth KO mice with normal diet (ND), and WT and LysM-Cre Fth KO mice with high-fat diet (HFD). These mice were analysed for characteristics of obesity and diabetes, tissue iron content, inflammation, oxidative stress, insulin sensitivity and metabolic measurements. RAW264.7 macrophage cells were used for in vitro experiments. Iron concentration reduced, and mRNA expression of ferroportin increased, in macrophages from LysM-Cre Fth KO mice. HFD-induced obesity was lower in LysM-Cre Fth KO mice than in WT mice at 12 weeks (body weight: KO 34.6 ± 5.6 g vs WT 40.1 ± 5.2 g). mRNA expression of inflammatory cytokines and infiltrated macrophages and oxidative stress increased in the adipose tissue of HFD-fed WT mice, but was not elevated in HFD-fed LysM-Cre Fth KO mice. However, WT mice fed an HFD had elevated iron concentration in adipose tissue and spleen, which was not observed in LysM-Cre Fth KO mice fed an HFD (adipose tissue [μmol Fe/g protein]: KO 1496 ± 479 vs WT 2316 ± 866; spleen [μmol Fe/g protein]: KO 218 ± 54 vs WT 334 ± 83). Moreover, HFD administration impaired both glucose tolerance and insulin sensitivity in WT mice, which was ameliorated in LysM-Cre Fth KO mice. In addition, energy expenditure, mRNA expression of thermogenic genes, and body temperature were higher in KO mice with HFD than WT mice with HFD. In vitro experiments showed that iron content was reduced, and lipopolysaccharide-induced Tnf-α (also known as Tnf) mRNA upregulation was inhibited in a macrophage cell line transfected with Fth siRNA. Deletion of macrophage H-ferritin suppresses the inflammatory response by reducing intracellular iron levels, resulting in the prevention of HFD-induced obesity and diabetes. The findings from this study highlight macrophage iron levels as a potential therapeutic target for obesity and diabetes.","ja":"Iron accumulation affects obesity and diabetes, both of which are ameliorated by iron reduction. Ferritin, an iron-storage protein, plays a crucial role in iron metabolism. H-ferritin exerts its cytoprotective action by reducing toxicity via its ferroxidase activity. We investigated the role of macrophage H-ferritin in obesity and diabetes. Conditional macrophage-specific H-ferritin (Fth, also known as Fth1) knockout (LysM-Cre Fth KO) mice were used and divided into four groups: wild-type (WT) and LysM-Cre Fth KO mice with normal diet (ND), and WT and LysM-Cre Fth KO mice with high-fat diet (HFD). These mice were analysed for characteristics of obesity and diabetes, tissue iron content, inflammation, oxidative stress, insulin sensitivity and metabolic measurements. RAW264.7 macrophage cells were used for in vitro experiments. Iron concentration reduced, and mRNA expression of ferroportin increased, in macrophages from LysM-Cre Fth KO mice. HFD-induced obesity was lower in LysM-Cre Fth KO mice than in WT mice at 12 weeks (body weight: KO 34.6 ± 5.6 g vs WT 40.1 ± 5.2 g). mRNA expression of inflammatory cytokines and infiltrated macrophages and oxidative stress increased in the adipose tissue of HFD-fed WT mice, but was not elevated in HFD-fed LysM-Cre Fth KO mice. However, WT mice fed an HFD had elevated iron concentration in adipose tissue and spleen, which was not observed in LysM-Cre Fth KO mice fed an HFD (adipose tissue [μmol Fe/g protein]: KO 1496 ± 479 vs WT 2316 ± 866; spleen [μmol Fe/g protein]: KO 218 ± 54 vs WT 334 ± 83). Moreover, HFD administration impaired both glucose tolerance and insulin sensitivity in WT mice, which was ameliorated in LysM-Cre Fth KO mice. In addition, energy expenditure, mRNA expression of thermogenic genes, and body temperature were higher in KO mice with HFD than WT mice with HFD. In vitro experiments showed that iron content was reduced, and lipopolysaccharide-induced Tnf-α (also known as Tnf) mRNA upregulation was inhibited in a macrophage cell line transfected with Fth siRNA. Deletion of macrophage H-ferritin suppresses the inflammatory response by reducing intracellular iron levels, resulting in the prevention of HFD-induced obesity and diabetes. The findings from this study highlight macrophage iron levels as a potential therapeutic target for obesity and diabetes."},"publication_date":"2020-07-11","publication_name":{"en":"Diabetologia","ja":"Diabetologia"},"volume":"Vol.63","number":"No.8","starting_page":"1588","ending_page":"1602","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1007/s00125-020-05153-0"],"issn":["1432-0428"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:24, {"insert":{"user_id":"B000337971","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/32307577","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=366414","label":"url"}],"paper_title":{"en":"Fibroblast-specific ERK5 deficiency changes tumor vasculature and exacerbates tumor progression in a mouse model.","ja":"Fibroblast-specific ERK5 deficiency changes tumor vasculature and exacerbates tumor progression in a mouse model."},"authors":{"en":[{"name":"Imanishi Masaki"},{"name":"Yamakawa Yusuke"},{"name":"Fukushima Keijo"},{"name":"Ikuto Raiki"},{"name":"Maegawa Akiko"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Horinouchi Yuya"},{"name":"Kondo Masateru"},{"name":"Kishuku Masatoshi"},{"name":"Goda Mitsuhiro"},{"name":"Zamami Yoshito"},{"name":"Takechi Kenshi"},{"name":"Chuma Masayuki"},{"name":"Ikeda Yasumasa"},{"name":"Tsuchiya Koichiro"},{"name":"Fujino Hiromichi"},{"name":"Tsuneyama Koichi"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"今西 正樹"},{"name":"Yamakawa Yusuke"},{"name":"福島 圭穣"},{"name":"生藤 来希"},{"name":"前川 晃子"},{"name":"石澤 有紀"},{"name":"堀ノ内 裕也"},{"name":"近藤 正輝"},{"name":"木宿 昌俊"},{"name":"合田 光寛"},{"name":"座間味 義人"},{"name":"武智 研志"},{"name":"中馬 真幸"},{"name":"池田 康将"},{"name":"土屋 浩一郎"},{"name":"藤野 裕道"},{"name":"常山 幸一"},{"name":"石澤 啓介"}]},"description":{"en":"The roles of cancer-associated fibroblasts (CAFs) have been studied in the tumor progression, and CAFs are expected to become the new targets for cancer pharmacotherapies. CAFs contribute to tumor cell survival and proliferation, tumor angiogenesis, immune suppression, tumor inflammation, tumor cell invasion and metastasis, and extracellular matrix remodeling. However, detailed mechanisms of how CAFs function in the living system remain unclear. CAFs include α-smooth muscle actin, expressing activated fibroblasts similar to myofibroblasts, and are highly capable of producing collagen. Several reports have demonstrated the contributions of extracellular-signal-regulated kinase 5 (ERK5) in fibroblasts to the fibrotic processes; however, the roles of CAF-derived ERK5 remain unclear. To investigate the roles of CAF-derived ERK5 in the tumor progression, we created mice lacking the ERK5 gene specifically in fibroblasts. Colon-26 mouse colon cancer cells were implanted into the mice subcutaneously, and the histological analyses of the tumor tissue were performed after 2 weeks. Immunofluorescence analyses showed that recipient-derived fibroblasts existed within the tumor tissue. The present study demonstrated that fibroblast-specific ERK5 deficiency exacerbated tumor progression and it was accompanied with thicker tumor vessel formation and the increase in the number of activated fibroblasts. We combined the results of The Cancer Genome Atlas (TCGA) database analysis with our animal studies, and indicated that regulating ERK5 activity in CAFs or CAF invasion into the tumor tissue can be important strategies for the development of new targets in cancer pharmacotherapies.","ja":"The roles of cancer-associated fibroblasts (CAFs) have been studied in the tumor progression, and CAFs are expected to become the new targets for cancer pharmacotherapies. CAFs contribute to tumor cell survival and proliferation, tumor angiogenesis, immune suppression, tumor inflammation, tumor cell invasion and metastasis, and extracellular matrix remodeling. However, detailed mechanisms of how CAFs function in the living system remain unclear. CAFs include α-smooth muscle actin, expressing activated fibroblasts similar to myofibroblasts, and are highly capable of producing collagen. Several reports have demonstrated the contributions of extracellular-signal-regulated kinase 5 (ERK5) in fibroblasts to the fibrotic processes; however, the roles of CAF-derived ERK5 remain unclear. To investigate the roles of CAF-derived ERK5 in the tumor progression, we created mice lacking the ERK5 gene specifically in fibroblasts. Colon-26 mouse colon cancer cells were implanted into the mice subcutaneously, and the histological analyses of the tumor tissue were performed after 2 weeks. Immunofluorescence analyses showed that recipient-derived fibroblasts existed within the tumor tissue. The present study demonstrated that fibroblast-specific ERK5 deficiency exacerbated tumor progression and it was accompanied with thicker tumor vessel formation and the increase in the number of activated fibroblasts. We combined the results of The Cancer Genome Atlas (TCGA) database analysis with our animal studies, and indicated that regulating ERK5 activity in CAFs or CAF invasion into the tumor tissue can be important strategies for the development of new targets in cancer pharmacotherapies."},"publication_date":"2020-04-19","publication_name":{"en":"Naunyn-Schmiedeberg's Archives of Pharmacology","ja":"Naunyn-Schmiedeberg's Archives of Pharmacology"},"volume":"Vol.393","number":"No.7","starting_page":"1239","ending_page":"1250","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1007/s00210-020-01859-5"],"issn":["1432-1912"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:25, {"insert":{"user_id":"B000337971","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/115530","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/31882204","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=366415","label":"url"}],"paper_title":{"en":"Rho-associated protein kinase and cyclophilin a are involved in inorganic phosphate-induced calcification signaling in vascular smooth muscle cells.","ja":"Rho-associated protein kinase and cyclophilin a are involved in inorganic phosphate-induced calcification signaling in vascular smooth muscle cells."},"authors":{"en":[{"name":"Tsuda Tatsuya"},{"name":"Imanishi Masaki"},{"name":"Oogoshi Mizuho"},{"name":"Goda Mitsuhiro"},{"name":"Kihira Yoshitaka"},{"name":"Horinouchi Yuya"},{"name":"Zamami Yoshito"},{"name":"Ishizawa Keisuke"},{"name":"Ikeda Yasumasa"},{"name":"Hashimoto Ichiro"},{"name":"Tamaki Toshiaki"},{"name":"Izawa-Ishizawa Yuki"}],"ja":[{"name":"津田 達也"},{"name":"今西 正樹"},{"name":"Oogoshi Mizuho"},{"name":"合田 光寛"},{"name":"木平 孝高"},{"name":"堀ノ内 裕也"},{"name":"座間味 義人"},{"name":"石澤 啓介"},{"name":"池田 康将"},{"name":"橋本 一郎"},{"name":"玉置 俊晃"},{"name":"石澤 有紀"}]},"description":{"en":"Arterial calcification, a risk factor of cardiovascular events, develops with differentiation of vascular smooth muscle cells (VSMCs) into osteoblast-like cells. Cyclophilin A (CypA) is a peptidyl-prolyl isomerase involved in cardiovascular diseases such as atherosclerosis and aortic aneurysms, and rho-associated protein kinase (ROCK) is involved in the pathogenesis of vascular calcification. CypA is secreted in a ROCK activity-dependent manner and works as a mitogen via autocrine or paracrine mechanisms in VSMCs. We examined the involvement of the ROCK-CypA axis in VSMC calcification induced by inorganic phosphate (Pi), a potent cell mineralization initiator. We found that Pi stimulated ROCK activity, CypA secretion, extracellular signal-regulated protein kinase (ERK) 1/2 phosphorylation, and runt-related transcription factor 2 expression, resulting in calcium accumulation in rat aortic smooth muscle cells (RASMCs). The ROCK inhibitor Y-27632 significantly suppressed Pi-induced CypA secretion, ERK1/2 phosphorylation, and calcium accumulation. Recombinant CypA was found to be associated with increased calcium accumulation in RASMCs. Based on these results, we suggest that autocrine CypA is mediated by ROCK activity and is involved in Pi-induced ERK1/2 phosphorylation following calcification signaling in RASMCs.","ja":"Arterial calcification, a risk factor of cardiovascular events, develops with differentiation of vascular smooth muscle cells (VSMCs) into osteoblast-like cells. Cyclophilin A (CypA) is a peptidyl-prolyl isomerase involved in cardiovascular diseases such as atherosclerosis and aortic aneurysms, and rho-associated protein kinase (ROCK) is involved in the pathogenesis of vascular calcification. CypA is secreted in a ROCK activity-dependent manner and works as a mitogen via autocrine or paracrine mechanisms in VSMCs. We examined the involvement of the ROCK-CypA axis in VSMC calcification induced by inorganic phosphate (Pi), a potent cell mineralization initiator. We found that Pi stimulated ROCK activity, CypA secretion, extracellular signal-regulated protein kinase (ERK) 1/2 phosphorylation, and runt-related transcription factor 2 expression, resulting in calcium accumulation in rat aortic smooth muscle cells (RASMCs). The ROCK inhibitor Y-27632 significantly suppressed Pi-induced CypA secretion, ERK1/2 phosphorylation, and calcium accumulation. Recombinant CypA was found to be associated with increased calcium accumulation in RASMCs. Based on these results, we suggest that autocrine CypA is mediated by ROCK activity and is involved in Pi-induced ERK1/2 phosphorylation following calcification signaling in RASMCs."},"publication_date":"2020-03","publication_name":{"en":"Journal of Pharmacological Sciences","ja":"Journal of Pharmacological Sciences"},"volume":"Vol.142","number":"No.3","starting_page":"109","ending_page":"115","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1016/j.jphs.2019.12.005"],"issn":["1347-8648"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:26, {"insert":{"user_id":"B000337971","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/113812","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/31669099","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=360423","label":"url"}],"paper_title":{"en":"Proton pump inhibitors block iron absorption through direct regulation of hepcidin via the aryl hydrocarbon receptor-mediated pathway","ja":"Proton pump inhibitors block iron absorption through direct regulation of hepcidin via the aryl hydrocarbon receptor-mediated pathway"},"authors":{"en":[{"name":"Hamano Hirofumi"},{"name":"Niimura Takahiro"},{"name":"Horinouchi Yuya"},{"name":"Zamami Yoshito"},{"name":"Takechi Kenshi"},{"name":"Goda Mitsuhiro"},{"name":"Imanishi Masaki"},{"name":"Chuma Masayuki"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Miyamoto Licht"},{"name":"Fukushima Keijo"},{"name":"Fujino Hiromichi"},{"name":"Tsuchiya Koichiro"},{"name":"Ishizawa Keisuke"},{"name":"Tamaki Toshiaki"},{"name":"Ikeda Yasumasa"}],"ja":[{"name":"濱野 裕章"},{"name":"新村 貴博"},{"name":"堀ノ内 裕也"},{"name":"座間味 義人"},{"name":"武智 研志"},{"name":"合田 光寛"},{"name":"今西 正樹"},{"name":"中馬 真幸"},{"name":"石澤 有紀"},{"name":"宮本 理人"},{"name":"福島 圭穣"},{"name":"藤野 裕道"},{"name":"土屋 浩一郎"},{"name":"石澤 啓介"},{"name":"玉置 俊晃"},{"name":"池田 康将"}]},"description":{"en":"Proton pump inhibitors (PPIs) have been used worldwide to treat gastrointestinal disorders. A recent study showed that long-term use of PPIs caused iron deficiency; however, it is unclear whether PPIs affect iron metabolism directly. We investigated the effect of PPIs on the peptide hepcidin, an important iron regulatory hormone. First, we used the FDA Adverse Event Reporting System database and analyzed the influence of PPIs. We found that PPIs, as well as H2 blockers, increased the odds ratio of iron-deficient anemia. Next, HepG2 cells were used to examine the action of PPIs and H2 blockers on hepcidin. PPIs augmented hepcidin expression, while H2 blockers did not. In fact, the PPI omeprazole increased hepcidin secretion, and omeprazole-induced hepcidin upregulation was inhibited by gene silencing or the pharmacological inhibition of the aryl hydrocarbon receptor. In mouse experiments, omeprazole also increased hepatic hepcidin mRNA expression and blood hepcidin levels. In mice treated with omeprazole, protein levels of duodenal and splenic ferroportin decreased. Taken together, PPIs directly affect iron metabolism by suppressing iron absorption through the inhibition of duodenal ferroportin via hepcidin upregulation. These findings provide a new insight into the molecular mechanism of PPI-induced iron deficiency.","ja":"Proton pump inhibitors (PPIs) have been used worldwide to treat gastrointestinal disorders. A recent study showed that long-term use of PPIs caused iron deficiency; however, it is unclear whether PPIs affect iron metabolism directly. We investigated the effect of PPIs on the peptide hepcidin, an important iron regulatory hormone. First, we used the FDA Adverse Event Reporting System database and analyzed the influence of PPIs. We found that PPIs, as well as H2 blockers, increased the odds ratio of iron-deficient anemia. Next, HepG2 cells were used to examine the action of PPIs and H2 blockers on hepcidin. PPIs augmented hepcidin expression, while H2 blockers did not. In fact, the PPI omeprazole increased hepcidin secretion, and omeprazole-induced hepcidin upregulation was inhibited by gene silencing or the pharmacological inhibition of the aryl hydrocarbon receptor. In mouse experiments, omeprazole also increased hepatic hepcidin mRNA expression and blood hepcidin levels. In mice treated with omeprazole, protein levels of duodenal and splenic ferroportin decreased. Taken together, PPIs directly affect iron metabolism by suppressing iron absorption through the inhibition of duodenal ferroportin via hepcidin upregulation. These findings provide a new insight into the molecular mechanism of PPI-induced iron deficiency."},"publication_date":"2020-01","publication_name":{"en":"Toxicology Letters","ja":"Toxicology Letters"},"volume":"Vol.318","starting_page":"86","ending_page":"91","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1016/j.toxlet.2019.10.016"],"issn":["1879-3169"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:27, {"insert":{"user_id":"B000337971","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/114461","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/31780928","label":"url"},{"@id":"https://www.scopus.com/record/display.url?eid=2-s2.0-85075592155&origin=inward","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=361105","label":"url"}],"paper_title":{"en":"Search for Therapeutic Agents for Cardiac Arrest Using a Drug Discovery Tool and Large-Scale Medical Information Database.","ja":"Search for Therapeutic Agents for Cardiac Arrest Using a Drug Discovery Tool and Large-Scale Medical Information Database."},"authors":{"en":[{"name":"Zamami Yoshito"},{"name":"Niimura Takahiro"},{"name":"Koyama Toshihiro"},{"name":"Shigemi Yuta"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Morita Mizuki"},{"name":"Ohshima Ayako"},{"name":"Harada Keisaku"},{"name":"Imai Toru"},{"name":"Hagiwara Hiromi"},{"name":"Okada Naoto"},{"name":"Goda Mitsuhiro"},{"name":"Takechi Kenshi"},{"name":"Chuma Masayuki"},{"name":"Kondo Yutaka"},{"name":"Tsuchiya Koichiro"},{"name":"Hinotsu Shiro"},{"name":"Kano Mitsunobu R"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"座間味 義人"},{"name":"新村 貴博"},{"name":"Koyama Toshihiro"},{"name":"Shigemi Yuta"},{"name":"石澤 有紀"},{"name":"Morita Mizuki"},{"name":"Ohshima Ayako"},{"name":"Harada Keisaku"},{"name":"Imai Toru"},{"name":"Hagiwara Hiromi"},{"name":"岡田 直人"},{"name":"合田 光寛"},{"name":"武智 研志"},{"name":"中馬 真幸"},{"name":"Kondo Yutaka"},{"name":"土屋 浩一郎"},{"name":"Hinotsu Shiro"},{"name":"Kano Mitsunobu R"},{"name":"石澤 啓介"}]},"description":{"en":"The survival rate of cardiac arrest patients is less than 10%; therefore, development of a therapeutic strategy that improves their prognosis is necessary. Herein, we searched data collected from medical facilities throughout Japan for drugs that improve the survival rate of cardiac arrest patients. Candidate drugs, which could improve the prognosis of cardiac arrest patients, were extracted using \"TargetMine,\" a drug discovery tool. We investigated whether the candidate drugs were among the drugs administered within 1 month after cardiac arrest in data of cardiac arrest cases obtained from the Japan Medical Data Center. Logistic regression analysis was performed, with the explanatory variables being the presence or absence of the administration of those candidate drugs that were administered to 10 patients and the objective variable being the \"survival discharge.\" Adjusted odds ratios for survival discharge were calculated using propensity scores for drugs that significantly improved the proportion of survival discharge; the influence of covariates, such as patient background, medical history, and treatment factors, was excluded by the inverse probability-of-treatment weighted method. Using the search strategy, we extracted 165 drugs with vasodilator activity as candidate drugs. Drugs not approved in Japan, oral medicines, and external medicines were excluded. Then, we investigated whether the candidate drugs were administered to the 2,227 cardiac arrest patients included in this study. The results of the logistic regression analysis showed that three (isosorbide dinitrate, nitroglycerin, and nicardipine) of seven drugs that were administered to 10 patients showed significant association with improvement in the proportion of survival discharge. Further analyses using propensity scores revealed that the adjusted odds ratios for survival discharge for patients administered isosorbide dinitrate, nitroglycerin, and nicardipine were 3.35, 5.44, and 4.58, respectively. Thus, it can be suggested that isosorbide dinitrate, nitroglycerin, and nicardipine could be novel therapeutic agents for improving the prognosis of cardiac arrest patients.","ja":"The survival rate of cardiac arrest patients is less than 10%; therefore, development of a therapeutic strategy that improves their prognosis is necessary. Herein, we searched data collected from medical facilities throughout Japan for drugs that improve the survival rate of cardiac arrest patients. Candidate drugs, which could improve the prognosis of cardiac arrest patients, were extracted using \"TargetMine,\" a drug discovery tool. We investigated whether the candidate drugs were among the drugs administered within 1 month after cardiac arrest in data of cardiac arrest cases obtained from the Japan Medical Data Center. Logistic regression analysis was performed, with the explanatory variables being the presence or absence of the administration of those candidate drugs that were administered to 10 patients and the objective variable being the \"survival discharge.\" Adjusted odds ratios for survival discharge were calculated using propensity scores for drugs that significantly improved the proportion of survival discharge; the influence of covariates, such as patient background, medical history, and treatment factors, was excluded by the inverse probability-of-treatment weighted method. Using the search strategy, we extracted 165 drugs with vasodilator activity as candidate drugs. Drugs not approved in Japan, oral medicines, and external medicines were excluded. Then, we investigated whether the candidate drugs were administered to the 2,227 cardiac arrest patients included in this study. The results of the logistic regression analysis showed that three (isosorbide dinitrate, nitroglycerin, and nicardipine) of seven drugs that were administered to 10 patients showed significant association with improvement in the proportion of survival discharge. Further analyses using propensity scores revealed that the adjusted odds ratios for survival discharge for patients administered isosorbide dinitrate, nitroglycerin, and nicardipine were 3.35, 5.44, and 4.58, respectively. Thus, it can be suggested that isosorbide dinitrate, nitroglycerin, and nicardipine could be novel therapeutic agents for improving the prognosis of cardiac arrest patients."},"publication_date":"2019-11-08","publication_name":{"en":"Frontiers in Pharmacology","ja":"Frontiers in Pharmacology"},"volume":"Vol.10","languages":["eng"],"referee":true,"identifiers":{"doi":["10.3389/fphar.2019.01257"],"issn":["1663-9812"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:28, {"insert":{"user_id":"B000337971","type":"published_papers","id":"30377886"},"force":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/31436802","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=358249","label":"url"}],"paper_title":{"en":"Factors Associated With Immune Checkpoint Inhibitor-Related Myocarditis.","ja":"Factors Associated With Immune Checkpoint Inhibitor-Related Myocarditis."},"authors":{"en":[{"name":"Zamami Yoshito"},{"name":"Niimura Takahiro"},{"name":"Okada Naoto"},{"name":"Koyama Toshihiro"},{"name":"Fukushima Keijo"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"座間味 義人"},{"name":"新村 貴博"},{"name":"岡田 直人"},{"name":"Koyama Toshihiro"},{"name":"福島 圭穣"},{"name":"石澤 有紀"},{"name":"石澤 啓介"}]},"publication_date":"2019-08-22","publication_name":{"en":"JAMA Oncology","ja":"JAMA Oncology"},"languages":["eng"],"referee":true,"identifiers":{"doi":["10.1001/jamaoncol.2019.3113"],"issn":["2374-2445"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:29, {"insert":{"user_id":"B000337971","type":"published_papers","id":"30377887"},"force":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/113746","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/31145863","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=351099","label":"url"}],"paper_title":{"en":"Iron accumulation causes impaired myogenesis correlated with MAPK signaling pathway inhibition by oxidative stress","ja":"Iron accumulation causes impaired myogenesis correlated with MAPK signaling pathway inhibition by oxidative stress"},"authors":{"en":[{"name":"Ikeda Yasumasa"},{"name":"Satoh Akiho"},{"name":"Horinouchi Yuya"},{"name":"Hamano Hirofumi"},{"name":"Watanabe Hiroaki"},{"name":"Imao Mizuki"},{"name":"Imanishi Masaki"},{"name":"Zamami Yoshito"},{"name":"Takechi Kenshi"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Miyamoto Licht"},{"name":"Tasuku Hirayama"},{"name":"Nagasawa Hideko"},{"name":"Ishizawa Keisuke"},{"name":"Aihara Ken-ichi"},{"name":"Tsuchiya Koichiro"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"池田 康将"},{"name":"佐藤 明穂"},{"name":"堀ノ内 裕也"},{"name":"濱野 裕章"},{"name":"渡邉 大晃"},{"name":"今尾 瑞季"},{"name":"今西 正樹"},{"name":"座間味 義人"},{"name":"武智 研志"},{"name":"石澤 有紀"},{"name":"宮本 理人"},{"name":"Tasuku Hirayama"},{"name":"永澤 秀子"},{"name":"石澤 啓介"},{"name":"粟飯原 賢一"},{"name":"土屋 浩一郎"},{"name":"玉置 俊晃"}]},"description":{"en":"Skeletal muscle atrophy is caused by disruption in the homeostatic balance of muscle degeneration and regeneration under various pathophysiological conditions. We have previously reported that iron accumulation induces skeletal muscle atrophy a ubiquitin ligase-dependent pathway. However, the potential effect of iron accumulation on muscle regeneration remains unclear. To examine the effect of iron accumulation on myogenesis, we used a mouse model with cardiotoxin (CTX)-induced muscle regeneration and C2C12 mouse myoblast cells . In mice with iron overload, the skeletal muscles exhibited increased oxidative stress and decreased expression of satellite cell markers. Following CTX-induced muscle injury, these mice also displayed delayed muscle regeneration with a decrease in the size of regenerating myofibers, reduced expression of myoblast differentiation markers, and decreased phosphorylation of MAPK signaling pathways. , iron overload also suppressed the differentiation of C2C12 myoblast cells but the suppression could be reversed by superoxide scavenging using tempol. Excess iron inhibits myogenesis oxidative stress, leading to an imbalance in skeletal muscle homeostasis.-Ikeda, Y., Satoh, A., Horinouchi, Y., Hamano, H., Watanabe, H., Imao, M., Imanishi, M., Zamami, Y., Takechi, K., Izawa-Ishizawa, Y., Miyamoto, L., Hirayama, T., Nagasawa, H., Ishizawa, K., Aihara, K.-I., Tsuchiya, K., Tamaki, T. Iron accumulation causes impaired myogenesis correlated with MAPK signaling pathway inhibition by oxidative stress.","ja":"Skeletal muscle atrophy is caused by disruption in the homeostatic balance of muscle degeneration and regeneration under various pathophysiological conditions. We have previously reported that iron accumulation induces skeletal muscle atrophy a ubiquitin ligase-dependent pathway. However, the potential effect of iron accumulation on muscle regeneration remains unclear. To examine the effect of iron accumulation on myogenesis, we used a mouse model with cardiotoxin (CTX)-induced muscle regeneration and C2C12 mouse myoblast cells . In mice with iron overload, the skeletal muscles exhibited increased oxidative stress and decreased expression of satellite cell markers. Following CTX-induced muscle injury, these mice also displayed delayed muscle regeneration with a decrease in the size of regenerating myofibers, reduced expression of myoblast differentiation markers, and decreased phosphorylation of MAPK signaling pathways. , iron overload also suppressed the differentiation of C2C12 myoblast cells but the suppression could be reversed by superoxide scavenging using tempol. Excess iron inhibits myogenesis oxidative stress, leading to an imbalance in skeletal muscle homeostasis.-Ikeda, Y., Satoh, A., Horinouchi, Y., Hamano, H., Watanabe, H., Imao, M., Imanishi, M., Zamami, Y., Takechi, K., Izawa-Ishizawa, Y., Miyamoto, L., Hirayama, T., Nagasawa, H., Ishizawa, K., Aihara, K.-I., Tsuchiya, K., Tamaki, T. Iron accumulation causes impaired myogenesis correlated with MAPK signaling pathway inhibition by oxidative stress."},"publication_date":"2019-08-01","publication_name":{"en":"The FASEB journal","ja":"The FASEB journal"},"volume":"Vol.33","number":"No.8","starting_page":"9551","ending_page":"9564","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1096/fj.201802724RR"],"issn":["1530-6860"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:30, {"insert":{"user_id":"B000337971","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/30062585","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=341569","label":"url"}],"paper_title":{"en":"Irinotecan-induced neutropenia is reduced by oral alkalization drugs: analysis using retrospective chart reviews and the spontaneous reporting database.","ja":"Irinotecan-induced neutropenia is reduced by oral alkalization drugs: analysis using retrospective chart reviews and the spontaneous reporting database."},"authors":{"en":[{"name":"Hamano Hirofumi"},{"name":"Mitsui Marin"},{"name":"Zamami Yoshito"},{"name":"Takechi Kenshi"},{"name":"Nimura Takahiro"},{"name":"Okada Naoto"},{"name":"Fukushima Keijo"},{"name":"Imanishi Masaki"},{"name":"Chuma Masayuki"},{"name":"Horinouchi Yuya"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Kirino Yasushi"},{"name":"Nakamura Toshimi"},{"name":"Teraoka Kazuhiko"},{"name":"Ikeda Yasumasa"},{"name":"Fujino Hiromichi"},{"name":"Yanagawa Hiroaki"},{"name":"Tamaki Toshiaki"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"濱野 裕章"},{"name":"三井 茉綸"},{"name":"座間味 義人"},{"name":"武智 研志"},{"name":"Nimura Takahiro"},{"name":"岡田 直人"},{"name":"福島 圭穣"},{"name":"今西 正樹"},{"name":"中馬 真幸"},{"name":"堀ノ内 裕也"},{"name":"石澤 有紀"},{"name":"Kirino Yasushi"},{"name":"Nakamura Toshimi"},{"name":"寺岡 和彦"},{"name":"池田 康将"},{"name":"藤野 裕道"},{"name":"楊河 宏章"},{"name":"玉置 俊晃"},{"name":"石澤 啓介"}]},"description":{"en":"These data indicate that oral alkalization drugs may reduce the frequency of neutropenia caused by irinotecan administration, making it possible to increase the dose safely.","ja":"These data indicate that oral alkalization drugs may reduce the frequency of neutropenia caused by irinotecan administration, making it possible to increase the dose safely."},"publication_date":"2019-03","publication_name":{"en":"Supportive Care in Cancer","ja":"Supportive Care in Cancer"},"volume":"Vol.27","number":"No.3","starting_page":"849","ending_page":"856","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1007/s00520-018-4367-y"],"issn":["1433-7339"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:31, {"insert":{"user_id":"B000337971","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/30351343","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=347373","label":"url"}],"paper_title":{"en":"Xanthine Oxidase Inhibition by Febuxostat in Macrophages Suppresses Angiotensin II-induced Aortic Fibrosis.","ja":"Xanthine Oxidase Inhibition by Febuxostat in Macrophages Suppresses Angiotensin II-induced Aortic Fibrosis."},"authors":{"en":[{"name":"Kondo Masateru"},{"name":"Imanishi Masaki"},{"name":"Fukushima Keijo"},{"name":"Ikuto Raiki"},{"name":"Murai Yoichi"},{"name":"Horinouchi Yuya"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Goda Mitsuhiro"},{"name":"Zamami Yoshito"},{"name":"Takechi Kenshi"},{"name":"Chuma Masayuki"},{"name":"Ikeda Yasumasa"},{"name":"Fujino Hiromichi"},{"name":"Tsuchiya Koichiro"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"近藤 正輝"},{"name":"今西 正樹"},{"name":"福島 圭穣"},{"name":"生藤 来希"},{"name":"村井 陽一"},{"name":"堀ノ内 裕也"},{"name":"石澤 有紀"},{"name":"合田 光寛"},{"name":"座間味 義人"},{"name":"武智 研志"},{"name":"中馬 真幸"},{"name":"池田 康将"},{"name":"藤野 裕道"},{"name":"土屋 浩一郎"},{"name":"石澤 啓介"}]},"description":{"en":"Our results suggested that FEB ameliorates Ang II-induced aortic fibrosis via suppressing macrophage-derived TGF-1 expression.","ja":"Our results suggested that FEB ameliorates Ang II-induced aortic fibrosis via suppressing macrophage-derived TGF-1 expression."},"publication_date":"2019-02-12","publication_name":{"en":"American Journal of Hypertension","ja":"American Journal of Hypertension"},"volume":"Vol.32","number":"No.3","starting_page":"249","ending_page":"256","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1093/ajh/hpy157"],"issn":["1941-7225"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:32, {"insert":{"user_id":"B000337971","type":"published_papers","id":"30377888"},"force":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/113264","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/30303488","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=347382","label":"url"}],"paper_title":{"en":"Development of a novel aortic dissection mouse model and evaluation of drug efficacy using in-vivo assays and database analyses.","ja":"Development of a novel aortic dissection mouse model and evaluation of drug efficacy using in-vivo assays and database analyses."},"authors":{"en":[{"name":"Izawa-Ishizawa Yuki"},{"name":"Imanishi Masaki"},{"name":"Zamami Yoshito"},{"name":"Hiroki Toya"},{"name":"Tomoko Nagao"},{"name":"Morishita Marin"},{"name":"Tsuneyama Koichi"},{"name":"Horinouchi Yuya"},{"name":"Kihira Yoshitaka"},{"name":"Takechi Kenshi"},{"name":"Ikeda Yasumasa"},{"name":"Tsuchiya Koichiro"},{"name":"Yoshizumi Masanori"},{"name":"Tamaki Toshiaki"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"石澤 有紀"},{"name":"今西 正樹"},{"name":"座間味 義人"},{"name":"戸谷 紘基"},{"name":"長尾 朋子"},{"name":"Morishita Marin"},{"name":"常山 幸一"},{"name":"堀ノ内 裕也"},{"name":"木平 孝高"},{"name":"武智 研志"},{"name":"池田 康将"},{"name":"土屋 浩一郎"},{"name":"吉栖 正典"},{"name":"玉置 俊晃"},{"name":"石澤 啓介"}]},"description":{"en":"Aortic dissection is a life-threatening disease. At present, the only therapeutic strategies available are surgery and antihypertensive drugs. Moreover, the molecular mechanisms underlying the onset of aortic dissection are still unclear. We established a novel aortic dissection model in mice using pharmacologically induced endothelial dysfunction. We then used the Japanese Adverse Drug Event Report database to investigate the role of pitavastatin in preventing the onset of aortic dissection. To induce endothelial dysfunction, Nω-nitro-L-arginine methyl ester, a nitric oxide synthase inhibitor, was administered to C57BL/6 mice. Three weeks later, angiotensin II (Ang II) and β-aminopropionitrile (BAPN), a lysyl oxidase inhibitor, were administered with osmotic mini-pumps. False lumen formation was used as the pathological determinant of aortic dissection. The incidences of aortic dissection and death from aneurysmal rupture were significantly higher in the Nω-nitro-L-arginine methyl ester, Ang II, and BAPN (LAB) group than they were in the Ang II and BAPN (AB) group.Pitavastatin was administered orally to LAB mice. It significantly lowered the incidences of dissection and rupture. It also decreased inflammation and medial degradation, both of which were exacerbated in the LAB group. The Japanese Adverse Drug Event Report database analysis indicated that there were 113 cases of aortic dissection out of 95 090 patients (0.12%) not receiving statins but only six cases out of 16 668 patients receiving statins (0.04%) (odds ratio: 0.30; P = 0.0043). Our results suggest that endothelial dysfunction is associated with the onset of aortic dissection and pitavastatin can help prevent this condition.","ja":"Aortic dissection is a life-threatening disease. At present, the only therapeutic strategies available are surgery and antihypertensive drugs. Moreover, the molecular mechanisms underlying the onset of aortic dissection are still unclear. We established a novel aortic dissection model in mice using pharmacologically induced endothelial dysfunction. We then used the Japanese Adverse Drug Event Report database to investigate the role of pitavastatin in preventing the onset of aortic dissection. To induce endothelial dysfunction, Nω-nitro-L-arginine methyl ester, a nitric oxide synthase inhibitor, was administered to C57BL/6 mice. Three weeks later, angiotensin II (Ang II) and β-aminopropionitrile (BAPN), a lysyl oxidase inhibitor, were administered with osmotic mini-pumps. False lumen formation was used as the pathological determinant of aortic dissection. The incidences of aortic dissection and death from aneurysmal rupture were significantly higher in the Nω-nitro-L-arginine methyl ester, Ang II, and BAPN (LAB) group than they were in the Ang II and BAPN (AB) group.Pitavastatin was administered orally to LAB mice. It significantly lowered the incidences of dissection and rupture. It also decreased inflammation and medial degradation, both of which were exacerbated in the LAB group. The Japanese Adverse Drug Event Report database analysis indicated that there were 113 cases of aortic dissection out of 95 090 patients (0.12%) not receiving statins but only six cases out of 16 668 patients receiving statins (0.04%) (odds ratio: 0.30; P = 0.0043). Our results suggest that endothelial dysfunction is associated with the onset of aortic dissection and pitavastatin can help prevent this condition."},"publication_date":"2019-01","publication_name":{"en":"Journal of Hypertension","ja":"Journal of Hypertension"},"volume":"Vol.37","number":"No.1","starting_page":"73","ending_page":"83","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1097/HJH.0000000000001898"],"issn":["1473-5598"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:33, {"insert":{"user_id":"B000337971","type":"published_papers","id":"30377889"},"force":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/30253416","label":"url"},{"@id":"https://www.scopus.com/record/display.url?eid=2-s2.0-85054191604&origin=inward","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=354050","label":"url"}],"paper_title":{"en":"Nitrosonifedipine, a Photodegradation Product of Nifedipine, Suppresses Pharmacologically Induced Aortic Aneurysm Formation.","ja":"Nitrosonifedipine, a Photodegradation Product of Nifedipine, Suppresses Pharmacologically Induced Aortic Aneurysm Formation."},"authors":{"en":[{"name":"Imanishi Masaki"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Sakurada T"},{"name":"Kohara Y"},{"name":"Horinouchi Yuya"},{"name":"Sairyo E"},{"name":"Zamami Yoshito"},{"name":"Takechi Kenshi"},{"name":"Chuma Masayuki"},{"name":"Fukushima Keijo"},{"name":"Ikeda Yasumasa"},{"name":"Fujino Hiromichi"},{"name":"Yoshizumi M"},{"name":"Tsuchiya Koichiro"},{"name":"Tamaki Toshiaki"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"今西 正樹"},{"name":"石澤 有紀"},{"name":"Sakurada T"},{"name":"Kohara Y"},{"name":"堀ノ内 裕也"},{"name":"Sairyo E"},{"name":"座間味 義人"},{"name":"武智 研志"},{"name":"中馬 真幸"},{"name":"福島 圭穣"},{"name":"池田 康将"},{"name":"藤野 裕道"},{"name":"Yoshizumi M"},{"name":"土屋 浩一郎"},{"name":"玉置 俊晃"},{"name":"石澤 啓介"}]},"description":{"en":"We have reported that nitrosonifedipine (NO-NIF), a photodegradation product of nifedipine, has strong antioxidant and endothelial protective effects, and can suppress several cardiovascular diseases in animal models. The objective of the present study was to investigate the effects of NO-NIF on aortic aneurysm formation. The mice were infused with β-aminopropionitrile for 2 weeks and angiotensin II for 6 weeks to induce aortic aneurysm formation. The oxidative stress was measured by dihydroethidium staining and nitrotyrosine staining. The expressions of inflammation-related genes were assessed by quantitative real-time PCR and immunohistochemical staining. To clarify the mechanisms of how NO-NIF suppresses vascular cell adhesion molecule (VCAM)-1, endothelial cells were used in in vitro system. NO-NIF suppressed pharmacologically induced the aortic aneurysm formation and aortic expansion without blood pressure changes. NO-NIF suppressed elastin degradation and matrix metalloproteinase-2 mRNA expression. NO-NIF suppressed the reactive oxygen species-cyclophilin A positive feedback loop. Upregulated mRNA expressions of inflammation-related genes and endothelial VCAM-1 were suppressed by NO-NIF co-treatment in aortae. NO-NIF has the potential to be a new, nifedipine-derived therapeutic drug for suppressing aortic aneurysm formation by directly improving aortic structure with its strong ability to reduce oxidative stress and inflammation.","ja":"We have reported that nitrosonifedipine (NO-NIF), a photodegradation product of nifedipine, has strong antioxidant and endothelial protective effects, and can suppress several cardiovascular diseases in animal models. The objective of the present study was to investigate the effects of NO-NIF on aortic aneurysm formation. The mice were infused with β-aminopropionitrile for 2 weeks and angiotensin II for 6 weeks to induce aortic aneurysm formation. The oxidative stress was measured by dihydroethidium staining and nitrotyrosine staining. The expressions of inflammation-related genes were assessed by quantitative real-time PCR and immunohistochemical staining. To clarify the mechanisms of how NO-NIF suppresses vascular cell adhesion molecule (VCAM)-1, endothelial cells were used in in vitro system. NO-NIF suppressed pharmacologically induced the aortic aneurysm formation and aortic expansion without blood pressure changes. NO-NIF suppressed elastin degradation and matrix metalloproteinase-2 mRNA expression. NO-NIF suppressed the reactive oxygen species-cyclophilin A positive feedback loop. Upregulated mRNA expressions of inflammation-related genes and endothelial VCAM-1 were suppressed by NO-NIF co-treatment in aortae. NO-NIF has the potential to be a new, nifedipine-derived therapeutic drug for suppressing aortic aneurysm formation by directly improving aortic structure with its strong ability to reduce oxidative stress and inflammation."},"publication_date":"2018-09-25","publication_name":{"en":"Pharmacology","ja":"Pharmacology"},"volume":"Vol.102","number":"No.5-6","starting_page":"281","ending_page":"286","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1159/000492577"],"issn":["1423-0313"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:34, {"insert":{"user_id":"B000337971","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/112445","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/30022146","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=342025","label":"url"}],"paper_title":{"en":"Renoprotective effects of a factor Xa inhibitor: fusion of basic research and a database analysis.","ja":"Renoprotective effects of a factor Xa inhibitor: fusion of basic research and a database analysis."},"authors":{"en":[{"name":"Horinouchi Yuya"},{"name":"Ikeda Yasumasa"},{"name":"Fukushima Keijo"},{"name":"Imanishi Masaki"},{"name":"Hamano Hirofumi"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Zamami Yoshito"},{"name":"Takechi Kenshi"},{"name":"Miyamoto Licht"},{"name":"Fujino Hiromichi"},{"name":"Ishizawa Keisuke"},{"name":"Tsuchiya Koichiro"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"堀ノ内 裕也"},{"name":"池田 康将"},{"name":"福島 圭穣"},{"name":"今西 正樹"},{"name":"Hamano Hirofumi"},{"name":"石澤 有紀"},{"name":"座間味 義人"},{"name":"武智 研志"},{"name":"宮本 理人"},{"name":"藤野 裕道"},{"name":"石澤 啓介"},{"name":"土屋 浩一郎"},{"name":"玉置 俊晃"}]},"description":{"en":"Renal tubulointerstitial injury, an inflammation-associated condition, is a major cause of chronic kidney disease (CKD). Levels of activated factor X (FXa), a blood coagulation factor, are increased in various inflammatory diseases. Therefore, we investigated the protective effects of an FXa inhibitor against renal tubulointerstitial injury using unilateral ureteral obstruction (UUO) mice (a renal tubulointerstitial fibrosis model) and the Food and Drug Administration Adverse Events Reporting System (FAERS) database. The renal expression levels of FX and the FXa receptors protease-activated receptor (PAR)-1 and PAR-2 were significantly higher in UUO mice than in sham-operated mice. UUO-induced tubulointerstitial fibrosis and extracellular matrix expression were suppressed in UUO mice treated with the FXa inhibitor edoxaban. Additionally, edoxaban attenuated UUO-induced macrophage infiltration and inflammatory molecule upregulation. In an analysis of the FAERS database, there were significantly fewer reports of tubulointerstitial nephritis for patients treated with FXa inhibitors than for patients not treated with inhibitors. These results suggest that FXa inhibitors exert protective effects against CKD by inhibiting tubulointerstitial fibrosis.","ja":"Renal tubulointerstitial injury, an inflammation-associated condition, is a major cause of chronic kidney disease (CKD). Levels of activated factor X (FXa), a blood coagulation factor, are increased in various inflammatory diseases. Therefore, we investigated the protective effects of an FXa inhibitor against renal tubulointerstitial injury using unilateral ureteral obstruction (UUO) mice (a renal tubulointerstitial fibrosis model) and the Food and Drug Administration Adverse Events Reporting System (FAERS) database. The renal expression levels of FX and the FXa receptors protease-activated receptor (PAR)-1 and PAR-2 were significantly higher in UUO mice than in sham-operated mice. UUO-induced tubulointerstitial fibrosis and extracellular matrix expression were suppressed in UUO mice treated with the FXa inhibitor edoxaban. Additionally, edoxaban attenuated UUO-induced macrophage infiltration and inflammatory molecule upregulation. In an analysis of the FAERS database, there were significantly fewer reports of tubulointerstitial nephritis for patients treated with FXa inhibitors than for patients not treated with inhibitors. These results suggest that FXa inhibitors exert protective effects against CKD by inhibiting tubulointerstitial fibrosis."},"publication_date":"2018-07-18","publication_name":{"en":"Scientific Reports","ja":"Scientific Reports"},"volume":"Vol.8","number":"No.1","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1038/s41598-018-29008-2"],"issn":["2045-2322"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:35, {"insert":{"user_id":"B000337971","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/110922","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/28992067","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=325682","label":"url"}],"paper_title":{"en":"The uremic toxin indoxyl sulfate interferes with iron metabolism by regulating hepcidin in chronic kidney disease","ja":"The uremic toxin indoxyl sulfate interferes with iron metabolism by regulating hepcidin in chronic kidney disease"},"authors":{"en":[{"name":"Hamano Hirofumi"},{"name":"Ikeda Yasumasa"},{"name":"Watanabe Hiroaki"},{"name":"Horinouchi Yuya"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Imanishi Masaki"},{"name":"Zamami Yoshito"},{"name":"Takechi Kenshi"},{"name":"Miyamoto Licht"},{"name":"Ishizawa Keisuke"},{"name":"Tsuchiya Koichiro"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"濱野 裕章"},{"name":"池田 康将"},{"name":"渡邉 大晃"},{"name":"堀ノ内 裕也"},{"name":"石澤 有紀"},{"name":"今西 正樹"},{"name":"座間味 義人"},{"name":"武智 研志"},{"name":"宮本 理人"},{"name":"石澤 啓介"},{"name":"土屋 浩一郎"},{"name":"玉置 俊晃"}]},"publication_date":"2018-04","publication_name":{"en":"Nephrology, Dialysis, Transplantation","ja":"Nephrology, Dialysis, Transplantation"},"volume":"Vol.33","number":"No.4","starting_page":"586","ending_page":"597","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1093/ndt/gfx252"],"issn":["1460-2385"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:36, {"insert":{"user_id":"B000337971","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/112397","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/29263333","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=335442","label":"url"}],"paper_title":{"en":"Hydrocortisone administration was associated with improved survival in Japanese patients with cardiac arrest.","ja":"Hydrocortisone administration was associated with improved survival in Japanese patients with cardiac arrest."},"authors":{"en":[{"name":"Niimura Takahiro"},{"name":"Zamami Yoshito"},{"name":"Koyama Toshihiro"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Miyake Masashi"},{"name":"Koga Tadashi"},{"name":"Harada Keisaku"},{"name":"Ohshima Ayako"},{"name":"Imai Toru"},{"name":"Kondo Yutaka"},{"name":"Imanishi Masaki"},{"name":"Takechi Kenshi"},{"name":"Fukushima Keijo"},{"name":"Horinouchi Yuya"},{"name":"Ikeda Yasumasa"},{"name":"Fujino Hiromichi"},{"name":"Tsuchiya Koichiro"},{"name":"Tamaki Toshiaki"},{"name":"Hinotsu Shiro"},{"name":"Kano Mitsunobu R"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"新村 貴博"},{"name":"座間味 義人"},{"name":"Koyama Toshihiro"},{"name":"石澤 有紀"},{"name":"Miyake Masashi"},{"name":"Koga Tadashi"},{"name":"Harada Keisaku"},{"name":"Ohshima Ayako"},{"name":"Imai Toru"},{"name":"Kondo Yutaka"},{"name":"今西 正樹"},{"name":"武智 研志"},{"name":"福島 圭穣"},{"name":"堀ノ内 裕也"},{"name":"池田 康将"},{"name":"藤野 裕道"},{"name":"土屋 浩一郎"},{"name":"玉置 俊晃"},{"name":"Hinotsu Shiro"},{"name":"Kano Mitsunobu R"},{"name":"石澤 啓介"}]},"description":{"en":"There are few reports on hydrocortisone administration after cardiac arrest, and those that have been published included few subjects. This study aimed to evaluate the effect of hydrocortisone administration on the outcomes of patients who experienced cardiac arrest. We investigated the survival discharge rates and the length of hospital stay from cardiac arrest to discharge, stratified by use of hydrocortisone, using a Japanese health-insurance claims dataset that covers approximately 2% of the Japanese population. The study included the data of 2233 subjects who experienced either in-hospital or out-of-hospital cardiac arrest between January 2005 and May 2014. These patients were divided into two groups, based on the administration of hydrocortisone. We adjusted the baseline characteristics, medical treatment, and drug administration data of the two groups using propensity scores obtained via the inverse probability of treatment weighted method. The hydrocortisone group had a significantly higher survival discharge rate (13/61 [21.1%] vs. 240/2172 [11.0%], adjusted odds ratio: 4.2, 95% CI: 1.60-10.98, p = 0.004). In addition, the administration of hydrocortisone was independent predictor of survival to discharge (hazard ratio: 4.6, p < 0.001). The results demonstrate a correlation between hydrocortisone administration and the high rates of survival to discharge.","ja":"There are few reports on hydrocortisone administration after cardiac arrest, and those that have been published included few subjects. This study aimed to evaluate the effect of hydrocortisone administration on the outcomes of patients who experienced cardiac arrest. We investigated the survival discharge rates and the length of hospital stay from cardiac arrest to discharge, stratified by use of hydrocortisone, using a Japanese health-insurance claims dataset that covers approximately 2% of the Japanese population. The study included the data of 2233 subjects who experienced either in-hospital or out-of-hospital cardiac arrest between January 2005 and May 2014. These patients were divided into two groups, based on the administration of hydrocortisone. We adjusted the baseline characteristics, medical treatment, and drug administration data of the two groups using propensity scores obtained via the inverse probability of treatment weighted method. The hydrocortisone group had a significantly higher survival discharge rate (13/61 [21.1%] vs. 240/2172 [11.0%], adjusted odds ratio: 4.2, 95% CI: 1.60-10.98, p = 0.004). In addition, the administration of hydrocortisone was independent predictor of survival to discharge (hazard ratio: 4.6, p < 0.001). The results demonstrate a correlation between hydrocortisone administration and the high rates of survival to discharge."},"publication_date":"2017-12-20","publication_name":{"en":"Scientific Reports","ja":"Scientific Reports"},"volume":"Vol.7","number":"No.1","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1038/s41598-017-17686-3"],"issn":["2045-2322"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:37, {"insert":{"user_id":"B000337971","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/112393","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/28978927","label":"url"},{"@id":"https://www.scopus.com/record/display.url?eid=2-s2.0-85030715238&origin=inward","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=334079","label":"url"}],"paper_title":{"en":"Meta-analysis of the efficacies of amiodarone and nifekalant in shock-resistant ventricular fibrillation and pulseless ventricular tachycardia.","ja":"Meta-analysis of the efficacies of amiodarone and nifekalant in shock-resistant ventricular fibrillation and pulseless ventricular tachycardia."},"authors":{"en":[{"name":"Sato Shiho"},{"name":"Zamami Yoshito"},{"name":"Imai Toru"},{"name":"Tanaka Satoshi"},{"name":"Koyama Toshihiro"},{"name":"Niimura Takahiro"},{"name":"Chuma Masayuki"},{"name":"Koga Tadashi"},{"name":"Takechi Kenshi"},{"name":"Kurata Yasuko"},{"name":"Kondo Yutaka"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Sendo Toshiaki"},{"name":"Nakura Hironori"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"Sato Shiho"},{"name":"座間味 義人"},{"name":"Imai Toru"},{"name":"Tanaka Satoshi"},{"name":"Koyama Toshihiro"},{"name":"新村 貴博"},{"name":"中馬 真幸"},{"name":"Koga Tadashi"},{"name":"武智 研志"},{"name":"Kurata Yasuko"},{"name":"Kondo Yutaka"},{"name":"石澤 有紀"},{"name":"Sendo Toshiaki"},{"name":"Nakura Hironori"},{"name":"石澤 啓介"}]},"description":{"en":"Amiodarone (AMD) and nifekalant (NIF) are used in the treatment of ventricular fibrillation or tachycardia; however, only few studies have been conducted on their efficacies. Therefore, a meta-analysis was conducted. Relevant sources were identified from PubMed, Cochrane Central Register of Controlled Trials, and Igaku Chuo Zasshi. The outcomes were short-term and long-term survival in patients with shock-resistant ventricular fibrillation /pulseless ventricular tachycardia. Thirty-three studies were analysed. The results showed that, compared to the control treatment, AMD did not improve short-term survival (odds ratio (OR): 1.25, 95% confidence interval (CI): 0.91-1.71) or long-term survival (OR: 1.00, 95% CI: 0.63-1.57). However, compared to the control treatment, NIF significantly improved short-term survival (OR: 3.23, 95% CI: 2.21-4.72) and long-term survival (OR: 1.88, 95% CI: 1.36-2.59). No significant difference was observed in short-term survival (OR: 0.85, 95% CI: 0.63-1.15) or long-term survival (OR: 1.25, 95% CI: 0.67-2.31) between AMD- and NIF-treated patients. The results suggest that NIF is beneficial for short-term and long-term survival in shock-resistant ventricular fibrillation/pulseless ventricular tachycardia; however, the efficacy of AMD in either outcome is not clear.","ja":"Amiodarone (AMD) and nifekalant (NIF) are used in the treatment of ventricular fibrillation or tachycardia; however, only few studies have been conducted on their efficacies. Therefore, a meta-analysis was conducted. Relevant sources were identified from PubMed, Cochrane Central Register of Controlled Trials, and Igaku Chuo Zasshi. The outcomes were short-term and long-term survival in patients with shock-resistant ventricular fibrillation /pulseless ventricular tachycardia. Thirty-three studies were analysed. The results showed that, compared to the control treatment, AMD did not improve short-term survival (odds ratio (OR): 1.25, 95% confidence interval (CI): 0.91-1.71) or long-term survival (OR: 1.00, 95% CI: 0.63-1.57). However, compared to the control treatment, NIF significantly improved short-term survival (OR: 3.23, 95% CI: 2.21-4.72) and long-term survival (OR: 1.88, 95% CI: 1.36-2.59). No significant difference was observed in short-term survival (OR: 0.85, 95% CI: 0.63-1.15) or long-term survival (OR: 1.25, 95% CI: 0.67-2.31) between AMD- and NIF-treated patients. The results suggest that NIF is beneficial for short-term and long-term survival in shock-resistant ventricular fibrillation/pulseless ventricular tachycardia; however, the efficacy of AMD in either outcome is not clear."},"publication_date":"2017-10-04","publication_name":{"en":"Scientific Reports","ja":"Scientific Reports"},"volume":"Vol.7","number":"No.1","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1038/s41598-017-13073-0"],"issn":["2045-2322"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:38, {"insert":{"user_id":"B000337971","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/112368","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/28878231","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=329173","label":"url"}],"paper_title":{"en":"Dietary iron restriction alleviates renal tubulointerstitial injury induced by protein overload in mice","ja":"Dietary iron restriction alleviates renal tubulointerstitial injury induced by protein overload in mice"},"authors":{"en":[{"name":"Ikeda Yasumasa"},{"name":"Horinouchi Yuya"},{"name":"Hirofumi Hamano"},{"name":"Tasuku Hirayama"},{"name":"Kishi Seiji"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Imanishi Masaki"},{"name":"Zamami Yoshito"},{"name":"Takechi Kenshi"},{"name":"Miyamoto Licht"},{"name":"Ishizawa Keisuke"},{"name":"Aihara Ken-ichi"},{"name":"Nagasawa Hideko"},{"name":"Tsuchiya Koichiro"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"池田 康将"},{"name":"堀ノ内 裕也"},{"name":"濱野 裕章"},{"name":"Tasuku Hirayama"},{"name":"岸 誠司"},{"name":"石澤 有紀"},{"name":"今西 正樹"},{"name":"座間味 義人"},{"name":"武智 研志"},{"name":"宮本 理人"},{"name":"石澤 啓介"},{"name":"粟飯原 賢一"},{"name":"永澤 秀子"},{"name":"土屋 浩一郎"},{"name":"玉置 俊晃"}]},"description":{"en":"Increased proteinuria causes tubulointerstitial injury due to inflammation in chronic kidney disease (CKD). Iron restriction exhibits protective effects against renal dysfunction; however, its effects against protein overload-induced tubulointerstitial damage remain unclear. Here, we investigated dietary iron restriction effect on tubulointerstitial damage in mice with protein-overload tubulointerstitial injury. Renal tubulointerstitial injury in animal model was induced by intraperitoneal injection of an overdose of bovine serum albumin (BSA). We divided mice into three groups: normal saline + normal diet (ND), BSA + ND, and BSA + iron-restricted diet (IRD). BSA overload induced renal tubulointerstitial injury in the ND mice, which was ameliorated in the IRD mice. Inflammatory cytokines and extracellular matrix mRNA expression was upregulated in BSA + ND mice kidneys and was inhibited by IRD. BSA-induced increase in renal superoxide production, NADPH oxidase activity, and p22(phox) expression was diminished in the IRD mice. IRD suppression increased BSA-induced renal macrophage infiltration. Moreover, BSA mice exhibited nucleotide-binding oligomerisation domain-like receptor pyrin domain-containing protein (NLRP) inflammasome activation, which was inhibited by IRD. Ferrous iron increased in kidneys with BSA overload and was inhibited by IRD. Thus, iron restriction inhibited oxidative stress and inflammatory changes, contributing to the protective effect against BSA overload-induced tubulointerstitial injury.","ja":"Increased proteinuria causes tubulointerstitial injury due to inflammation in chronic kidney disease (CKD). Iron restriction exhibits protective effects against renal dysfunction; however, its effects against protein overload-induced tubulointerstitial damage remain unclear. Here, we investigated dietary iron restriction effect on tubulointerstitial damage in mice with protein-overload tubulointerstitial injury. Renal tubulointerstitial injury in animal model was induced by intraperitoneal injection of an overdose of bovine serum albumin (BSA). We divided mice into three groups: normal saline + normal diet (ND), BSA + ND, and BSA + iron-restricted diet (IRD). BSA overload induced renal tubulointerstitial injury in the ND mice, which was ameliorated in the IRD mice. Inflammatory cytokines and extracellular matrix mRNA expression was upregulated in BSA + ND mice kidneys and was inhibited by IRD. BSA-induced increase in renal superoxide production, NADPH oxidase activity, and p22(phox) expression was diminished in the IRD mice. IRD suppression increased BSA-induced renal macrophage infiltration. Moreover, BSA mice exhibited nucleotide-binding oligomerisation domain-like receptor pyrin domain-containing protein (NLRP) inflammasome activation, which was inhibited by IRD. Ferrous iron increased in kidneys with BSA overload and was inhibited by IRD. Thus, iron restriction inhibited oxidative stress and inflammatory changes, contributing to the protective effect against BSA overload-induced tubulointerstitial injury."},"publication_date":"2017-09-06","publication_name":{"en":"Scientific Reports","ja":"Scientific Reports"},"volume":"Vol.7","number":"No.1","starting_page":"10621","ending_page":"10621","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1038/s41598-017-11089-0"],"issn":["2045-2322"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:39, {"insert":{"user_id":"B000337971","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/113749","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/28263291","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=322994","label":"url"}],"paper_title":{"en":"Iron suppresses erythropoietin expression via oxidative stress-dependent hypoxia-inducible factor-2 alpha inactivation","ja":"Iron suppresses erythropoietin expression via oxidative stress-dependent hypoxia-inducible factor-2 alpha inactivation"},"authors":{"en":[{"name":"Oshima Keisuke"},{"name":"Ikeda Yasumasa"},{"name":"Horinouchi Yuya"},{"name":"Watanabe Hiroaki"},{"name":"Hamano Hirofumi"},{"name":"Kihira Yoshitaka"},{"name":"Kishi Seiji"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Miyamoto Licht"},{"name":"Hirayama Tasuku"},{"name":"Nagasawa Hideko"},{"name":"Ishizawa Keisuke"},{"name":"Tsuchiya Koichiro"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"大島 啓亮"},{"name":"池田 康将"},{"name":"堀ノ内 裕也"},{"name":"Watanabe Hiroaki"},{"name":"Hamano Hirofumi"},{"name":"木平 孝高"},{"name":"岸 誠司"},{"name":"石澤 有紀"},{"name":"宮本 理人"},{"name":"Hirayama Tasuku"},{"name":"永澤 秀子"},{"name":"石澤 啓介"},{"name":"土屋 浩一郎"},{"name":"玉置 俊晃"}]},"description":{"en":"Renal anemia is a major complication in chronic kidney disease (CKD). Iron supplementation, as well as erythropoiesis-stimulating agents, are widely used for treatment of renal anemia. However, excess iron causes oxidative stress via the Fenton reaction, and iron supplementation might damage remnant renal function including erythropoietin (EPO) production in CKD. EPO gene expression was suppressed in mice following direct iron treatment. Hypoxia-inducible factor-2 alpha (HIF-2α), a positive regulator of the EPO gene, was also diminished in the kidney of mice following iron treatment. Anemia-induced increase in renal EPO and HIF-2α expression was inhibited by iron treatment. In in vitro experiments using EPO-producing HepG2 cells, iron stimulation reduced the expression of the EPO gene, as well as HIF-2α. Moreover, iron treatment augmented oxidative stress, and iron-induced reduction of EPO and HIF-2α expression was restored by tempol, an antioxidant compound. HIF-2α interaction with the Epo promoter was inhibited by iron treatment, and was restored by tempol. These findings suggested that iron supplementation reduced EPO gene expression via an oxidative stress-HIF-2α-dependent signaling pathway.","ja":"Renal anemia is a major complication in chronic kidney disease (CKD). Iron supplementation, as well as erythropoiesis-stimulating agents, are widely used for treatment of renal anemia. However, excess iron causes oxidative stress via the Fenton reaction, and iron supplementation might damage remnant renal function including erythropoietin (EPO) production in CKD. EPO gene expression was suppressed in mice following direct iron treatment. Hypoxia-inducible factor-2 alpha (HIF-2α), a positive regulator of the EPO gene, was also diminished in the kidney of mice following iron treatment. Anemia-induced increase in renal EPO and HIF-2α expression was inhibited by iron treatment. In in vitro experiments using EPO-producing HepG2 cells, iron stimulation reduced the expression of the EPO gene, as well as HIF-2α. Moreover, iron treatment augmented oxidative stress, and iron-induced reduction of EPO and HIF-2α expression was restored by tempol, an antioxidant compound. HIF-2α interaction with the Epo promoter was inhibited by iron treatment, and was restored by tempol. These findings suggested that iron supplementation reduced EPO gene expression via an oxidative stress-HIF-2α-dependent signaling pathway."},"publication_date":"2017-03-06","publication_name":{"en":"Laboratory Investigation; a Journal of Technical Methods and Pathology","ja":"Laboratory Investigation; a Journal of Technical Methods and Pathology"},"volume":"Vol.97","number":"No.5","starting_page":"555","ending_page":"566","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1038/labinvest.2017.11"],"issn":["1530-0307"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:40, {"insert":{"user_id":"B000337971","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/110118","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/28090711","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=323552","label":"url"}],"paper_title":{"en":"Topical Application of Nitrosonifedipine, a Novel Radical Scavenger, Ameliorates Ischemic Skin Flap Necrosis in a Mouse Model.","ja":"Topical Application of Nitrosonifedipine, a Novel Radical Scavenger, Ameliorates Ischemic Skin Flap Necrosis in a Mouse Model."},"authors":{"en":[{"name":"Fukunaga Yutaka"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Horinouchi Yuya"},{"name":"Sairyo Eriko"},{"name":"Ikeda Yasumasa"},{"name":"Ishizawa Keisuke"},{"name":"Tsuchiya Koichiro"},{"name":"Abe Yoshiro"},{"name":"Hashimoto Ichiro"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"福永 豊"},{"name":"石澤 有紀"},{"name":"堀ノ内 裕也"},{"name":"Sairyo Eriko"},{"name":"池田 康将"},{"name":"石澤 啓介"},{"name":"土屋 浩一郎"},{"name":"安倍 吉郎"},{"name":"橋本 一郎"},{"name":"玉置 俊晃"}]},"description":{"en":"Ischemic skin flap necrosis can occur in random pattern flaps. An excess amount of reactive oxygen species is generated and causes necrosis in the ischemic tissue. Nitrosonifedipine (NO-NIF) has been demonstrated to possess potent radical scavenging ability. However, there has been no study on the effects of NO-NIF on ischemic skin flap necrosis. Therefore, they evaluated the potential of NO-NIF in ameliorating ischemic skin flap necrosis in a mouse model. A random pattern skin flap (1.0 × 3.0 cm) was elevated on the dorsum of C57BL/6 mice. NO-NIF was administered by topical injection immediately after surgery and every 24 hours thereafter. Flap survival was evaluated on postoperative day 7. Tissue samples from the skin flaps were harvested on postoperative days 1 and 3 to analyze oxidative stress, apoptosis and endothelial dysfunction. The viable area of the flap in the NO-NIF group was significantly increased (78.30 ± 7.041%) compared with that of the control group (47.77 ± 6.549%, p < 0.01). NO-NIF reduced oxidative stress, apoptosis and endothelial dysfunction, which were evidenced by the decrease of malondialdehyde, p22phox protein expression, number of apoptotic cells, phosphorylated p38 MAPK protein expression, and vascular cell adhesion molecule-1 protein expression while endothelial nitric oxide synthase protein expression was increased. In conclusion, they demonstrated that NO-NIF ameliorated ischemic skin flap necrosis by reducing oxidative stress, apoptosis, and endothelial dysfunction. NO-NIF is considered to be a candidate for the treatment of ischemic flap necrosis.","ja":"Ischemic skin flap necrosis can occur in random pattern flaps. An excess amount of reactive oxygen species is generated and causes necrosis in the ischemic tissue. Nitrosonifedipine (NO-NIF) has been demonstrated to possess potent radical scavenging ability. However, there has been no study on the effects of NO-NIF on ischemic skin flap necrosis. Therefore, they evaluated the potential of NO-NIF in ameliorating ischemic skin flap necrosis in a mouse model. A random pattern skin flap (1.0 × 3.0 cm) was elevated on the dorsum of C57BL/6 mice. NO-NIF was administered by topical injection immediately after surgery and every 24 hours thereafter. Flap survival was evaluated on postoperative day 7. Tissue samples from the skin flaps were harvested on postoperative days 1 and 3 to analyze oxidative stress, apoptosis and endothelial dysfunction. The viable area of the flap in the NO-NIF group was significantly increased (78.30 ± 7.041%) compared with that of the control group (47.77 ± 6.549%, p < 0.01). NO-NIF reduced oxidative stress, apoptosis and endothelial dysfunction, which were evidenced by the decrease of malondialdehyde, p22phox protein expression, number of apoptotic cells, phosphorylated p38 MAPK protein expression, and vascular cell adhesion molecule-1 protein expression while endothelial nitric oxide synthase protein expression was increased. In conclusion, they demonstrated that NO-NIF ameliorated ischemic skin flap necrosis by reducing oxidative stress, apoptosis, and endothelial dysfunction. NO-NIF is considered to be a candidate for the treatment of ischemic flap necrosis."},"publication_date":"2017-02-17","publication_name":{"en":"Wound Repair and Regeneration","ja":"Wound Repair and Regeneration"},"volume":"Vol.25","number":"No.2","starting_page":"217","ending_page":"223","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1111/wrr.12510"],"issn":["1524-475X"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:41, {"insert":{"user_id":"B000337971","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/113750","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/27049128","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=306466","label":"url"}],"paper_title":{"en":"Iron-induced skeletal muscle atrophy involves an Akt-forkhead box O3-E3 ubiquitin ligase-dependent pathway","ja":"Iron-induced skeletal muscle atrophy involves an Akt-forkhead box O3-E3 ubiquitin ligase-dependent pathway"},"authors":{"en":[{"name":"Ikeda Yasumasa"},{"name":"Imao Mizuki"},{"name":"Satoh Akiho"},{"name":"Watanabe Hiroaki"},{"name":"Hamano Hirofumi"},{"name":"Horinouchi Yuya"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Kihira Yoshitaka"},{"name":"Miyamoto Licht"},{"name":"Ishizawa Keisuke"},{"name":"Tsuchiya Koichiro"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"池田 康将"},{"name":"今尾 瑞季"},{"name":"佐藤 明穂"},{"name":"渡邉 大晃"},{"name":"濱野 裕章"},{"name":"堀ノ内 裕也"},{"name":"石澤 有紀"},{"name":"木平 孝高"},{"name":"宮本 理人"},{"name":"石澤 啓介"},{"name":"土屋 浩一郎"},{"name":"玉置 俊晃"}]},"description":{"en":"Skeletal muscle wasting or sarcopenia is a critical health problem. Skeletal muscle atrophy is induced by an excess of iron, which is an essential trace metal for all living organisms. Excessive amounts of iron catalyze the formation of highly toxic hydroxyl radicals via the Fenton reaction. However, the molecular mechanism of iron-induced skeletal muscle atrophy has remained unclear. In this study, 8-weeks-old C57BL6/J mice were divided into 2 groups: vehicle-treated group and the iron-injected group (10 mg iron·day-1·mouse-1) during 2 weeks. Mice in the iron-injected group showed an increase in the iron content of the skeletal muscle and serum and ferritin levels in the muscle, along with reduced skeletal muscle mass. The skeletal muscle showed elevated mRNA expression of the muscle atrophy-related E3 ubiquitin ligases, atrogin-1 and muscle ring finger-1(MuRF1), on days 7 and 14 of iron treatment. Moreover, iron-treated mice showed reduced phosphorylation of Akt and forkhead box O3 (FOXO3a) in skeletal muscles. Inhibition of FOXO3a using siRNA in vitro in C2C12 myotube cells inhibited iron-induced upregulation of atrogin-1 and MuRF1 and reversed the reduction in myotube diameters. Iron-load caused oxidative stress, and an oxidative stress inhibitor abrogated iron-induced muscle atrophy by reactivating the Akt-FOXO3 pathway. Iron-induced skeletal muscle atrophy is suggested to involve the E3 ubiquitin ligase mediated by the reduction of Akt-FOXO3a signaling by oxidative stress.","ja":"Skeletal muscle wasting or sarcopenia is a critical health problem. Skeletal muscle atrophy is induced by an excess of iron, which is an essential trace metal for all living organisms. Excessive amounts of iron catalyze the formation of highly toxic hydroxyl radicals via the Fenton reaction. However, the molecular mechanism of iron-induced skeletal muscle atrophy has remained unclear. In this study, 8-weeks-old C57BL6/J mice were divided into 2 groups: vehicle-treated group and the iron-injected group (10 mg iron·day-1·mouse-1) during 2 weeks. Mice in the iron-injected group showed an increase in the iron content of the skeletal muscle and serum and ferritin levels in the muscle, along with reduced skeletal muscle mass. The skeletal muscle showed elevated mRNA expression of the muscle atrophy-related E3 ubiquitin ligases, atrogin-1 and muscle ring finger-1(MuRF1), on days 7 and 14 of iron treatment. Moreover, iron-treated mice showed reduced phosphorylation of Akt and forkhead box O3 (FOXO3a) in skeletal muscles. Inhibition of FOXO3a using siRNA in vitro in C2C12 myotube cells inhibited iron-induced upregulation of atrogin-1 and MuRF1 and reversed the reduction in myotube diameters. Iron-load caused oxidative stress, and an oxidative stress inhibitor abrogated iron-induced muscle atrophy by reactivating the Akt-FOXO3 pathway. Iron-induced skeletal muscle atrophy is suggested to involve the E3 ubiquitin ligase mediated by the reduction of Akt-FOXO3a signaling by oxidative stress."},"publication_date":"2016-05","publication_name":{"en":"Journal of Trace Elements in Medicine and Biology","ja":"Journal of Trace Elements in Medicine and Biology"},"volume":"Vol.35","number":"No.5","starting_page":"66","ending_page":"76","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1016/j.jtemb.2016.01.011"],"issn":["1878-3252"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:42, {"insert":{"user_id":"B000337971","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/113751","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/26134126","label":"url"},{"@id":"https://www.scopus.com/record/display.url?eid=2-s2.0-84946558014&origin=inward","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=294522","label":"url"}],"paper_title":{"en":"Bilirubin exerts pro-angiogenic effects through an Akt-eNOS-dependent pathway","ja":"Bilirubin exerts pro-angiogenic effects through an Akt-eNOS-dependent pathway"},"authors":{"en":[{"name":"Ikeda Yasumasa"},{"name":"Hamano Hirofumi"},{"name":"Satoh Akiho"},{"name":"Horinouchi Yuya"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Kihira Yoshitaka"},{"name":"Ishizawa Keisuke"},{"name":"Aihara Ken-ichi"},{"name":"Tsuchiya Koichiro"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"池田 康将"},{"name":"濱野 裕章"},{"name":"佐藤 明穂"},{"name":"堀ノ内 裕也"},{"name":"石澤 有紀"},{"name":"木平 孝高"},{"name":"石澤 啓介"},{"name":"粟飯原 賢一"},{"name":"土屋 浩一郎"},{"name":"玉置 俊晃"}]},"description":{"en":"Low serum bilirubin levels are associated with the risk of cardiovascular diseases including peripheral artery disease. Bilirubin is known to exert its property such as antioxidant effect or the enhancement of flow-mediated vasodilation, however, bilirubin action on angiogenesis remains unclear. To investigate the molecular mechanism of bilirubin on angiogenic effect, we first employed C57BL/6J mice with unilateral hindlimb ischemia surgery and divided the mice into two groups (vehicle-treated group and bilirubin-treated group). The analysis of laser speckle blood flow demonstrated the enhancement of blood flow recovery in response to ischemia of mice with bilirubin treatment. The density of capillaries was significantly higher in ischemic-adductor muscles of bilirubin-treated mice. The phosphorylated levels of endothelial nitric oxide synthase (eNOS) and Akt were increased in ischemic skeletal muscles of mice with bilirubin treatment compared with vehicle treatment. In in vitro experiments by using human aortic endothelial cells, bilirubin augmented eNOS and Akt phosphorylation, cell proliferation, cell migration and tube formation. These bilirubin actions on endothelial cell activation were inhibited by LY294002, a phosphatidylinositol 3-kinase inhibitor. In conclusion, bilirubin promotes angiogenesis through endothelial cells activation via Akt-eNOS-dependent manner.","ja":"Low serum bilirubin levels are associated with the risk of cardiovascular diseases including peripheral artery disease. Bilirubin is known to exert its property such as antioxidant effect or the enhancement of flow-mediated vasodilation, however, bilirubin action on angiogenesis remains unclear. To investigate the molecular mechanism of bilirubin on angiogenic effect, we first employed C57BL/6J mice with unilateral hindlimb ischemia surgery and divided the mice into two groups (vehicle-treated group and bilirubin-treated group). The analysis of laser speckle blood flow demonstrated the enhancement of blood flow recovery in response to ischemia of mice with bilirubin treatment. The density of capillaries was significantly higher in ischemic-adductor muscles of bilirubin-treated mice. The phosphorylated levels of endothelial nitric oxide synthase (eNOS) and Akt were increased in ischemic skeletal muscles of mice with bilirubin treatment compared with vehicle treatment. In in vitro experiments by using human aortic endothelial cells, bilirubin augmented eNOS and Akt phosphorylation, cell proliferation, cell migration and tube formation. These bilirubin actions on endothelial cell activation were inhibited by LY294002, a phosphatidylinositol 3-kinase inhibitor. In conclusion, bilirubin promotes angiogenesis through endothelial cells activation via Akt-eNOS-dependent manner."},"publication_date":"2015-07-02","publication_name":{"en":"Hypertension Research","ja":"Hypertension Research"},"volume":"Vol.38","number":"No.11","starting_page":"733","ending_page":"740","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1038/hr.2015.74"],"issn":["1348-4214"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:43, {"insert":{"user_id":"B000337971","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/113753","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/25096756","label":"url"},{"@id":"https://www.scopus.com/record/display.url?eid=2-s2.0-84937513465&origin=inward","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=280180","label":"url"}],"paper_title":{"en":"Angiotensin II alters the expression of duodenal iron transporters, hepatic hepcidin, and body iron distribution in mice","ja":"Angiotensin II alters the expression of duodenal iron transporters, hepatic hepcidin, and body iron distribution in mice"},"authors":{"en":[{"name":"Tajima Soichiro"},{"name":"Ikeda Yasumasa"},{"name":"Enomoto Hideaki"},{"name":"Imao Mizuki"},{"name":"Horinouchi Yuya"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Kihira Yoshitaka"},{"name":"Miyamoto Licht"},{"name":"Ishizawa Keisuke"},{"name":"Tsuchiya Koichiro"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"Tajima Soichiro"},{"name":"池田 康将"},{"name":"榎本 英明"},{"name":"今尾 瑞季"},{"name":"堀ノ内 裕也"},{"name":"石澤 有紀"},{"name":"木平 孝高"},{"name":"宮本 理人"},{"name":"石澤 啓介"},{"name":"土屋 浩一郎"},{"name":"玉置 俊晃"}]},"description":{"en":"Angiotensin II (ANG II) has been shown to affect iron metabolism through alteration of iron transporters, leading to increased cellular and tissue iron contents. Serum ferritin, a marker of body iron storage, is elevated in various cardiovascular diseases, including hypertension. However, the associated changes in iron absorption and the mechanism underlying increased iron content in a hypertensive state remain unclear. The C57BL6/J mice were treated with ANG II to generate a model of hypertension. Mice were divided into three groups: (1) control, (2) ANG II-treated, and (3) ANG II-treated and ANG II receptor blocker (ARB)-administered (ANG II-ARB) groups. Mice treated with ANG II showed increased serum ferritin levels compared to vehicle-treated control mice. In ANG II-treated mice, duodenal divalent metal transporter-1 and ferroportin (FPN) expression levels were increased and hepatic hepcidin mRNA expression and serum hepcidin concentration were reduced. The mRNA expression of bone morphogenetic protein 6 and CCAAT/enhancer-binding protein alpha, which are regulators of hepcidin, was also down-regulated in the livers of ANG II-treated mice. In terms of tissue iron content, macrophage iron content and renal iron content were increased by ANG II treatment, and these increases were associated with reduced expression of transferrin receptor 1 and FPN and increased expression of ferritin. These changes induced by ANG II treatment were ameliorated by the administration of an ARB. Angiotensin II (ANG II) altered the expression of duodenal iron transporters and reduced hepcidin levels, contributing to the alteration of body iron distribution.","ja":"Angiotensin II (ANG II) has been shown to affect iron metabolism through alteration of iron transporters, leading to increased cellular and tissue iron contents. Serum ferritin, a marker of body iron storage, is elevated in various cardiovascular diseases, including hypertension. However, the associated changes in iron absorption and the mechanism underlying increased iron content in a hypertensive state remain unclear. The C57BL6/J mice were treated with ANG II to generate a model of hypertension. Mice were divided into three groups: (1) control, (2) ANG II-treated, and (3) ANG II-treated and ANG II receptor blocker (ARB)-administered (ANG II-ARB) groups. Mice treated with ANG II showed increased serum ferritin levels compared to vehicle-treated control mice. In ANG II-treated mice, duodenal divalent metal transporter-1 and ferroportin (FPN) expression levels were increased and hepatic hepcidin mRNA expression and serum hepcidin concentration were reduced. The mRNA expression of bone morphogenetic protein 6 and CCAAT/enhancer-binding protein alpha, which are regulators of hepcidin, was also down-regulated in the livers of ANG II-treated mice. In terms of tissue iron content, macrophage iron content and renal iron content were increased by ANG II treatment, and these increases were associated with reduced expression of transferrin receptor 1 and FPN and increased expression of ferritin. These changes induced by ANG II treatment were ameliorated by the administration of an ARB. Angiotensin II (ANG II) altered the expression of duodenal iron transporters and reduced hepcidin levels, contributing to the alteration of body iron distribution."},"publication_date":"2015-07","publication_name":{"en":"European Journal of Nutrition","ja":"European Journal of Nutrition"},"volume":"Vol.54","number":"No.5","starting_page":"709","ending_page":"719","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1007/s00394-014-0749-1"],"issn":["1436-6215"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:44, {"insert":{"user_id":"B000337971","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/109948","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/25832631","label":"url"},{"@id":"https://cir.nii.ac.jp/crid/1390001204631777920/","label":"url"},{"@id":"https://www.scopus.com/record/display.url?eid=2-s2.0-84928951796&origin=inward","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=289231","label":"url"}],"paper_title":{"en":"Hypoxia decreases glucagon-like peptide-1 secretion from GLUTag cell line","ja":"Hypoxia decreases glucagon-like peptide-1 secretion from GLUTag cell line"},"authors":{"en":[{"name":"Kihira Yoshitaka"},{"name":"Burentogtokh Ariunzaya"},{"name":"Itoh Mari"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Ishizawa Keisuke"},{"name":"Ikeda Yasumasa"},{"name":"Tsuchiya Koichiro"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"木平 孝高"},{"name":"Burentogtokh Ariunzaya"},{"name":"Itoh Mari"},{"name":"石澤 有紀"},{"name":"石澤 啓介"},{"name":"池田 康将"},{"name":"土屋 浩一郎"},{"name":"玉置 俊晃"}]},"description":{"en":"Glucagon-like peptide-1 (GLP-1), an incretin hormone, is secreted from L cells located in the intestinal epithelium. It is known that intestinal oxygen tension is decreased postprandially. In addition, we found that the expression of hypoxia-inducible factor-1α (HIF-1α), which accumulates in cells under hypoxic conditions, was significantly increased in the colons of mice with food intake, indicating that the oxygen concentration is likely reduced in the colon after eating. Therefore, we hypothesized that GLP-1 secretion is affected by oxygen tension. We found that forskolin-stimulated GLP-1 secretion from GLUTag cells, a model of intestinal L cells, is suppressed in hypoxia (1% O2). Forskolin-stimulated elevations of preproglucagon (ppGCG) and proprotein convertase 1/3 (PC1/3) mRNA expression were decreased under hypoxic conditions. The finding that H89, a protein kinase A (PKA) inhibitor, inhibited the forskolin-stimulated increase of ppGCG and PC1/3 indicated that the cAMP-PKA pathway is involved in the hypoxia-induced suppression of the genes. Hypoxia decreased hexokinase 2 mRNA and protein expression and increased lactate dehydrogenase A mRNA and protein expression. Concomitantly, lactate production was increased and ATP production was decreased. Together, the results indicate that hypoxia decreases glucose utilization for ATP production, which probably causes a decrease in cAMP production and in subsequent GLP-1 production. Our findings suggest that the postprandial decrease in oxygen tension in the intestine attenuates GLP-1 secretion.","ja":"Glucagon-like peptide-1 (GLP-1), an incretin hormone, is secreted from L cells located in the intestinal epithelium. It is known that intestinal oxygen tension is decreased postprandially. In addition, we found that the expression of hypoxia-inducible factor-1α (HIF-1α), which accumulates in cells under hypoxic conditions, was significantly increased in the colons of mice with food intake, indicating that the oxygen concentration is likely reduced in the colon after eating. Therefore, we hypothesized that GLP-1 secretion is affected by oxygen tension. We found that forskolin-stimulated GLP-1 secretion from GLUTag cells, a model of intestinal L cells, is suppressed in hypoxia (1% O2). Forskolin-stimulated elevations of preproglucagon (ppGCG) and proprotein convertase 1/3 (PC1/3) mRNA expression were decreased under hypoxic conditions. The finding that H89, a protein kinase A (PKA) inhibitor, inhibited the forskolin-stimulated increase of ppGCG and PC1/3 indicated that the cAMP-PKA pathway is involved in the hypoxia-induced suppression of the genes. Hypoxia decreased hexokinase 2 mRNA and protein expression and increased lactate dehydrogenase A mRNA and protein expression. Concomitantly, lactate production was increased and ATP production was decreased. Together, the results indicate that hypoxia decreases glucose utilization for ATP production, which probably causes a decrease in cAMP production and in subsequent GLP-1 production. Our findings suggest that the postprandial decrease in oxygen tension in the intestine attenuates GLP-1 secretion."},"publication_date":"2015-04","publication_name":{"en":"Biological & Pharmaceutical Bulletin","ja":"Biological & Pharmaceutical Bulletin"},"volume":"Vol.38","number":"No.4","starting_page":"514","ending_page":"521","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1248/bpb.b14-00612"],"issn":["1347-5215"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:45, {"insert":{"user_id":"B000337971","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"http://ci.nii.ac.jp/naid/40020377946/","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/25994136","label":"url"},{"@id":"https://cir.nii.ac.jp/crid/1390282681302013696/","label":"url"},{"@id":"https://www.scopus.com/record/display.url?eid=2-s2.0-84929747372&origin=inward","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=288751","label":"url"}],"paper_title":{"en":"A Long-Term High-Fat Diet Changes Iron Distribution in Body, Increasing Iron Accumulation Specifically in the Mouse Spleen","ja":"A Long-Term High-Fat Diet Changes Iron Distribution in Body, Increasing Iron Accumulation Specifically in the Mouse Spleen"},"authors":{"en":[{"name":"Yamano Noriko"},{"name":"Ikeda Yasumasa"},{"name":"Sakama Minoru"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Kihira Yoshitaka"},{"name":"Ishizawa Keisuke"},{"name":"Miyamoto Licht"},{"name":"Tomita Shuhei"},{"name":"Tsuchiya Koichiro"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"山野 範子"},{"name":"池田 康将"},{"name":"阪間 稔"},{"name":"石澤 有紀"},{"name":"木平 孝高"},{"name":"石澤 啓介"},{"name":"宮本 理人"},{"name":"冨田 修平"},{"name":"土屋 浩一郎"},{"name":"玉置 俊晃"}]},"description":{"en":"Although iron is an essential trace metal, its presence in excess causes oxidative stress in the human body. Recent studies have indicated that iron storage is a risk factor for type 2 diabetes mellitus. Dietary iron restriction or iron chelation ameliorates symptoms of type 2 diabetes in mouse models. However, whether iron content in the body changes with the development of diabetes is unknown. Here, we investigated the dynamics of iron accumulation and changes in iron absorption-related genes in mice that developed obesity and diabetes by consuming a high-fat diet (HFD-fed mice). HFD-fed mice (18-20 wk) were compared with control mice for hematologic features, serum ferritin levels, and iron contents in the gastrocnemius muscle, heart, epididymal fat, testis, liver, duodenum, and spleen. In addition, the spleen was examined histologically. Iron absorption-related gene expression in the liver and duodenum was also examined. Hemoglobin and serum ferritin levels were increased in HFD-fed mice. The HFD-fed mice showed iron accumulation in the spleen, but not in the heart or liver. Increased percentages of the splenic red pulp and macrophages were observed in HFD-fed mice and iron accumulation in the spleen was found mainly in the splenic red pulp. The HFD-fed mice also showed decreased iron content in the duodenum. The mRNA expression of divalent metal transporter-1 (DMT-1), an iron absorption-related gene, was elevated in the duodenum of HFD-fed mice. These results indicate that iron accumulation (specifically accumulation in the spleen) is enhanced by the development of type 2 diabetes induced by HFD.","ja":"Although iron is an essential trace metal, its presence in excess causes oxidative stress in the human body. Recent studies have indicated that iron storage is a risk factor for type 2 diabetes mellitus. Dietary iron restriction or iron chelation ameliorates symptoms of type 2 diabetes in mouse models. However, whether iron content in the body changes with the development of diabetes is unknown. Here, we investigated the dynamics of iron accumulation and changes in iron absorption-related genes in mice that developed obesity and diabetes by consuming a high-fat diet (HFD-fed mice). HFD-fed mice (18-20 wk) were compared with control mice for hematologic features, serum ferritin levels, and iron contents in the gastrocnemius muscle, heart, epididymal fat, testis, liver, duodenum, and spleen. In addition, the spleen was examined histologically. Iron absorption-related gene expression in the liver and duodenum was also examined. Hemoglobin and serum ferritin levels were increased in HFD-fed mice. The HFD-fed mice showed iron accumulation in the spleen, but not in the heart or liver. Increased percentages of the splenic red pulp and macrophages were observed in HFD-fed mice and iron accumulation in the spleen was found mainly in the splenic red pulp. The HFD-fed mice also showed decreased iron content in the duodenum. The mRNA expression of divalent metal transporter-1 (DMT-1), an iron absorption-related gene, was elevated in the duodenum of HFD-fed mice. These results indicate that iron accumulation (specifically accumulation in the spleen) is enhanced by the development of type 2 diabetes induced by HFD."},"publication_date":"2015-03","publication_name":{"en":"Journal of Nutritional Science and Vitaminology","ja":"Journal of Nutritional Science and Vitaminology"},"volume":"Vol.61","number":"No.1","starting_page":"20","ending_page":"27","languages":["eng"],"referee":true,"identifiers":{"doi":["10.3177/jnsv.61.20"],"issn":["0301-4800"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:46, {"insert":{"user_id":"B000337971","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/25187658","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=286621","label":"url"}],"paper_title":{"en":"Identification of Activators of ERK5 Transcriptional Activity by High-Throughput Screening and the Role of Endothelial ERK5 in Vasoprotective Effects Induced by Statins and Antimalarial Agents.","ja":"Identification of Activators of ERK5 Transcriptional Activity by High-Throughput Screening and the Role of Endothelial ERK5 in Vasoprotective Effects Induced by Statins and Antimalarial Agents."},"authors":{"en":[{"name":"Le Nhat-Tu"},{"name":"Takei Yuichiro"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Heo Kyung-Sun"},{"name":"Lee Hakjoo"},{"name":"Smrcka Alan V"},{"name":"Miller Benjamin L"},{"name":"Ko Kyung Ae"},{"name":"Ture Sara"},{"name":"Morrell Craig"},{"name":"Fujiwara Keigi"},{"name":"Akaike Masashi"},{"name":"Abe Jun-Ichi"}],"ja":[{"name":"Le Nhat-Tu"},{"name":"Takei Yuichiro"},{"name":"石澤 有紀"},{"name":"Heo Kyung-Sun"},{"name":"Lee Hakjoo"},{"name":"Smrcka Alan V"},{"name":"Miller Benjamin L"},{"name":"Ko Kyung Ae"},{"name":"Ture Sara"},{"name":"Morrell Craig"},{"name":"Fujiwara Keigi"},{"name":"赤池 雅史"},{"name":"Abe Jun-Ichi"}]},"description":{"en":"Because ERK5 inhibits endothelial inflammation and dysfunction, activating ERK5 might be a novel approach to protecting vascular endothelial cells (ECs) against various pathological conditions of the blood vessel. We have identified small molecules that protect ECs via ERK5 activation and determined their contribution to preventing cardiac allograft rejection. Using high-throughput screening, we identified certain statins and antimalarial agents including chloroquine, hydroxychloroquine, and quinacrine as strong ERK5 activators. Pitavastatin enhanced ERK5 transcriptional activity and Kruppel-like factor-2 expression in cultured human and bovine ECs, but these effects were abolished by the depletion of ERK5. Chloroquine and hydroxychloroquine upregulated ERK5 kinase activity and inhibited VCAM-1 expression in an ERK5-dependent but MAPK/ERK kinase 5- and Kruppel-like factor 2/4-independent manner. Leukocyte rolling and vascular reactivity were used to evaluate endothelial function in vivo, and we found that EC-specific ERK5 knockout (ERK5-EKO) mice exhibited increased leukocyte rolling and impaired vascular reactivity, which could not be corrected by pitavastatin. The role of endothelial ERK5 in acute cardiac allograft rejection was also examined by heterotopic grafting of the heart obtained from either wild-type or ERK5-EKO mice into allomismatched recipient mice. A robust increase in both inflammatory gene expression and CD45-positive cell infiltration into the graft was observed. These tissue rejection responses were inhibited by pitavastatin in wild-type but not ERK5-EKO hearts. Our study has identified statins and antimalarial drugs as strong ERK5 activators and shown that ERK5 activation is preventive of endothelial inflammation and dysfunction and acute allograft rejection.","ja":"Because ERK5 inhibits endothelial inflammation and dysfunction, activating ERK5 might be a novel approach to protecting vascular endothelial cells (ECs) against various pathological conditions of the blood vessel. We have identified small molecules that protect ECs via ERK5 activation and determined their contribution to preventing cardiac allograft rejection. Using high-throughput screening, we identified certain statins and antimalarial agents including chloroquine, hydroxychloroquine, and quinacrine as strong ERK5 activators. Pitavastatin enhanced ERK5 transcriptional activity and Kruppel-like factor-2 expression in cultured human and bovine ECs, but these effects were abolished by the depletion of ERK5. Chloroquine and hydroxychloroquine upregulated ERK5 kinase activity and inhibited VCAM-1 expression in an ERK5-dependent but MAPK/ERK kinase 5- and Kruppel-like factor 2/4-independent manner. Leukocyte rolling and vascular reactivity were used to evaluate endothelial function in vivo, and we found that EC-specific ERK5 knockout (ERK5-EKO) mice exhibited increased leukocyte rolling and impaired vascular reactivity, which could not be corrected by pitavastatin. The role of endothelial ERK5 in acute cardiac allograft rejection was also examined by heterotopic grafting of the heart obtained from either wild-type or ERK5-EKO mice into allomismatched recipient mice. A robust increase in both inflammatory gene expression and CD45-positive cell infiltration into the graft was observed. These tissue rejection responses were inhibited by pitavastatin in wild-type but not ERK5-EKO hearts. Our study has identified statins and antimalarial drugs as strong ERK5 activators and shown that ERK5 activation is preventive of endothelial inflammation and dysfunction and acute allograft rejection."},"publication_date":"2014-09-03","publication_name":{"en":"The Journal of Immunology","ja":"The Journal of Immunology"},"volume":"Vol.193","number":"No.7","starting_page":"3803","ending_page":"3815","languages":["eng"],"referee":true,"identifiers":{"doi":["10.4049/jimmunol.1400571"],"issn":["1550-6606"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:47, {"insert":{"user_id":"B000337971","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/106145","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/24623277","label":"url"},{"@id":"https://www.scopus.com/record/display.url?eid=2-s2.0-84901457818&origin=inward","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=275488","label":"url"}],"paper_title":{"en":"Smooth muscle cell specific Hif-1 deficiency suppresses angiotensin II-induced vascular remodeling in mice","ja":"Smooth muscle cell specific Hif-1 deficiency suppresses angiotensin II-induced vascular remodeling in mice"},"authors":{"en":[{"name":"Imanishi Masaki"},{"name":"Tomita Shuhei"},{"name":"Ishizawa Keisuke"},{"name":"Kihira Yoshitaka"},{"name":"Ueno Masaki"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Ikeda Yasumasa"},{"name":"Yamano Noriko"},{"name":"Tsuchiya Koichiro"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"今西 正樹"},{"name":"冨田 修平"},{"name":"石澤 啓介"},{"name":"木平 孝高"},{"name":"Ueno Masaki"},{"name":"石澤 有紀"},{"name":"池田 康将"},{"name":"山野 範子"},{"name":"土屋 浩一郎"},{"name":"玉置 俊晃"}]},"description":{"en":"Vascular remodelling is mediated by vascular smooth muscle cell (VSMC) proliferation and hypertrophy, both processes of which are linked to medial thickening and fibrosis. Here, we show that hypoxia-inducible factor-1α (Hif-1α) expressed in smooth muscle cells (SMCs) is involved in angiotensin II (Ang II)-induced vascular remodelling in an in vivo model. To clarify the role of Hif-1α in vascular remodelling, we created mice lacking the Hif-1α gene in SMCs (SMKO mice). Ang II infusion induced medial thickening and vascular fibrosis, accompanied by Hif-1α up-regulation, in the aortae of control mice, but not in those of SMKO mice. In accordance with those results, our in vitro studies showed that the deletion of SMC-derived Hif-1α suppressed the Ang II-induced hypertrophy of VSMCs, and our in vivo studies showed that the Ang II-induced expression of fibrosis-related genes in aortae was suppressed by SMC-specific Hif-1α deficiency. In addition, the SMC-specific Hif-1α deficiency suppressed Ang II-induced macrophage infiltration and Ang II-induced expression of inflammation-related genes in aortae. The superoxide production observed in the aortae of control mice with Ang II was suppressed in those of SMKO mice with Ang II, and this finding was consistent with the results of little Ang II-induced c-Src phosphorylation in SMKO mouse aortae. Loss- and gain-of-function analysis in in vitro experiments confirmed that VSMC-derived Hif-1α functions as an intrinsic modulator of vascular remodelling-related gene expression. Our results revealed that SMC-derived Hif-1α is a crucial mediator of Ang II-induced vascular remodelling.","ja":"Vascular remodelling is mediated by vascular smooth muscle cell (VSMC) proliferation and hypertrophy, both processes of which are linked to medial thickening and fibrosis. Here, we show that hypoxia-inducible factor-1α (Hif-1α) expressed in smooth muscle cells (SMCs) is involved in angiotensin II (Ang II)-induced vascular remodelling in an in vivo model. To clarify the role of Hif-1α in vascular remodelling, we created mice lacking the Hif-1α gene in SMCs (SMKO mice). Ang II infusion induced medial thickening and vascular fibrosis, accompanied by Hif-1α up-regulation, in the aortae of control mice, but not in those of SMKO mice. In accordance with those results, our in vitro studies showed that the deletion of SMC-derived Hif-1α suppressed the Ang II-induced hypertrophy of VSMCs, and our in vivo studies showed that the Ang II-induced expression of fibrosis-related genes in aortae was suppressed by SMC-specific Hif-1α deficiency. In addition, the SMC-specific Hif-1α deficiency suppressed Ang II-induced macrophage infiltration and Ang II-induced expression of inflammation-related genes in aortae. The superoxide production observed in the aortae of control mice with Ang II was suppressed in those of SMKO mice with Ang II, and this finding was consistent with the results of little Ang II-induced c-Src phosphorylation in SMKO mouse aortae. Loss- and gain-of-function analysis in in vitro experiments confirmed that VSMC-derived Hif-1α functions as an intrinsic modulator of vascular remodelling-related gene expression. Our results revealed that SMC-derived Hif-1α is a crucial mediator of Ang II-induced vascular remodelling."},"publication_date":"2014-06","publication_name":{"en":"Cardiovascular Research","ja":"Cardiovascular Research"},"volume":"Vol.102","number":"No.3","starting_page":"460","ending_page":"468","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1093/cvr/cvu061"],"issn":["0008-6363"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:48, {"insert":{"user_id":"B000337971","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/106138","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/25289325","label":"url"},{"@id":"https://www.scopus.com/record/display.url?eid=2-s2.0-84897362750&origin=inward","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=286620","label":"url"}],"paper_title":{"en":"Overexpressed HIF-2α in Endothelial Cells Promotes Vascularization and Improves Random Pattern Skin Flap Survival.","ja":"Overexpressed HIF-2α in Endothelial Cells Promotes Vascularization and Improves Random Pattern Skin Flap Survival."},"authors":{"en":[{"name":"Morimoto Atsushi"},{"name":"Tomita Shuhei"},{"name":"Imanishi Masaki"},{"name":"Shioi Go"},{"name":"Kihira Yoshitaka"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Takaku Mitsuru"},{"name":"Hashimoto Ichiro"},{"name":"Ikeda Yasumasa"},{"name":"Nakanishi Hideki"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"森本 篤志"},{"name":"冨田 修平"},{"name":"今西 正樹"},{"name":"Shioi Go"},{"name":"木平 孝高"},{"name":"石澤 有紀"},{"name":"Takaku Mitsuru"},{"name":"橋本 一郎"},{"name":"池田 康将"},{"name":"中西 秀樹"},{"name":"玉置 俊晃"}]},"description":{"en":"Specific overexpression of HIF-2 in ECs promoted vascularization and enhanced skin flap survival in vivo in a mouse model.","ja":"Specific overexpression of HIF-2 in ECs promoted vascularization and enhanced skin flap survival in vivo in a mouse model."},"publication_date":"2014-05-07","publication_name":{"en":"Plastic and Reconstructive Surgery. Global Open","ja":"Plastic and Reconstructive Surgery. Global Open"},"volume":"Vol.2","number":"No.4","starting_page":"e132","ending_page":"e132","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1097/GOX.0000000000000083"],"issn":["2169-7574"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:49, {"insert":{"user_id":"B000337971","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/24705496","label":"url"},{"@id":"https://www.scopus.com/record/display.url?eid=2-s2.0-84899440448&origin=inward","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=276331","label":"url"}],"paper_title":{"en":"Deletion of hypoxia-inducible factor-1α in adipocytes enhances glucagon-like peptide-1 secretion and reduces adipose tissue inflammation.","ja":"Deletion of hypoxia-inducible factor-1α in adipocytes enhances glucagon-like peptide-1 secretion and reduces adipose tissue inflammation."},"authors":{"en":[{"name":"Kihira Yoshitaka"},{"name":"Miyake Mariko"},{"name":"Hirata Manami"},{"name":"Hoshina Yoji"},{"name":"Kato Kana"},{"name":"Shirakawa Hitoshi"},{"name":"Sakaue Hiroshi"},{"name":"Yamano Noriko"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Ishizawa Keisuke"},{"name":"Ikeda Yasumasa"},{"name":"Tsuchiya Koichiro"},{"name":"Tamaki Toshiaki"},{"name":"Tomita Shuhei"}],"ja":[{"name":"木平 孝高"},{"name":"Miyake Mariko"},{"name":"Hirata Manami"},{"name":"Hoshina Yoji"},{"name":"Kato Kana"},{"name":"Shirakawa Hitoshi"},{"name":"阪上 浩"},{"name":"山野 範子"},{"name":"石澤 有紀"},{"name":"石澤 啓介"},{"name":"池田 康将"},{"name":"土屋 浩一郎"},{"name":"玉置 俊晃"},{"name":"冨田 修平"}]},"description":{"en":"It is known that obese adipose tissues are hypoxic and express hypoxia-inducible factor (HIF)-1α. Although some studies have shown that the expression of HIF-1α in adipocytes induces glucose intolerance, the mechanisms are still not clear. In this study, we examined its effects on the development of type 2 diabetes by using adipocyte-specific HIF-1α knockout (ahKO) mice. ahKO mice showed improved glucose tolerance compared with wild type (WT) mice. Macrophage infiltration and mRNA levels of monocyte chemotactic protein-1 (MCP-1) and tumor necrosis factor α (TNFα) were decreased in the epididymal adipose tissues of high fat diet induced obese ahKO mice. The results indicated that the obesity-induced adipose tissue inflammation was suppressed in ahKO mice. In addition, in the ahKO mice, serum insulin levels were increased under the free-feeding but not the fasting condition, indicating that postprandial insulin secretion was enhanced. Serum glucagon-like peptide-1 (GLP-1) levels were also increased in the ahKO mice. Interestingly, adiponectin, whose serum levels were increased in the obese ahKO mice compared with the obese WT mice, stimulated GLP-1 secretion from cultured intestinal L cells. Therefore, insulin secretion may have been enhanced through the adiponectin-GLP-1 pathway in the ahKO mice. Our results suggest that the deletion of HIF-1α in adipocytes improves glucose tolerance by enhancing insulin secretion through the GLP-1 pathway and by reducing macrophage infiltration and inflammation in adipose tissue.","ja":"It is known that obese adipose tissues are hypoxic and express hypoxia-inducible factor (HIF)-1α. Although some studies have shown that the expression of HIF-1α in adipocytes induces glucose intolerance, the mechanisms are still not clear. In this study, we examined its effects on the development of type 2 diabetes by using adipocyte-specific HIF-1α knockout (ahKO) mice. ahKO mice showed improved glucose tolerance compared with wild type (WT) mice. Macrophage infiltration and mRNA levels of monocyte chemotactic protein-1 (MCP-1) and tumor necrosis factor α (TNFα) were decreased in the epididymal adipose tissues of high fat diet induced obese ahKO mice. The results indicated that the obesity-induced adipose tissue inflammation was suppressed in ahKO mice. In addition, in the ahKO mice, serum insulin levels were increased under the free-feeding but not the fasting condition, indicating that postprandial insulin secretion was enhanced. Serum glucagon-like peptide-1 (GLP-1) levels were also increased in the ahKO mice. Interestingly, adiponectin, whose serum levels were increased in the obese ahKO mice compared with the obese WT mice, stimulated GLP-1 secretion from cultured intestinal L cells. Therefore, insulin secretion may have been enhanced through the adiponectin-GLP-1 pathway in the ahKO mice. Our results suggest that the deletion of HIF-1α in adipocytes improves glucose tolerance by enhancing insulin secretion through the GLP-1 pathway and by reducing macrophage infiltration and inflammation in adipose tissue."},"publication_date":"2014-04-04","publication_name":{"en":"PLoS ONE","ja":"PLoS ONE"},"volume":"Vol.9","number":"No.4","starting_page":"e93856","ending_page":"e93856","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1371/journal.pone.0093856"],"issn":["1932-6203"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:50, {"insert":{"user_id":"B000337971","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/113752","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/24586712","label":"url"},{"@id":"https://www.scopus.com/record/display.url?eid=2-s2.0-84897786390&origin=inward","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=274493","label":"url"}],"paper_title":{"en":"Iron chelation by deferoxamine prevents renal interstitial fibrosis in mice with unilateral ureteral obstruction","ja":"Iron chelation by deferoxamine prevents renal interstitial fibrosis in mice with unilateral ureteral obstruction"},"authors":{"en":[{"name":"Ikeda Yasumasa"},{"name":"Ozono Iori"},{"name":"Tajima Soichro"},{"name":"Imao Mizuki"},{"name":"Horinouchi Yuya"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Kihira Yoshitaka"},{"name":"Miyamoto Licht"},{"name":"Ishizawa Keisuke"},{"name":"Tsuchiya Koichiro"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"池田 康将"},{"name":"大園 伊織"},{"name":"Tajima Soichro"},{"name":"今尾 瑞季"},{"name":"堀ノ内 裕也"},{"name":"石澤 有紀"},{"name":"木平 孝高"},{"name":"宮本 理人"},{"name":"石澤 啓介"},{"name":"土屋 浩一郎"},{"name":"玉置 俊晃"}]},"description":{"en":"Renal fibrosis plays an important role in the onset and progression of chronic kidney diseases (CKD). Although several mechanisms underlying renal fibrosis and candidate drugs for its treatment have been identified, the effect of iron chelator on renal fibrosis remains unclear. In the present study, we examined the effect of an iron chelator, deferoxamine (DFO), on renal fibrosis in mice with surgically induced unilateral ureter obstruction (UUO). Mice were divided into 4 groups: UUO with vehicle, UUO with DFO, sham with vehicle, and sham with DFO. One week after surgery, augmented renal tubulointerstitial fibrosis and the expression of collagen I, III, and IV increased in mice with UUO; these changes were suppressed by DFO treatment. Similarly, UUO-induced macrophage infiltration of renal interstitial tubules was reduced in UUO mice treated with DFO. UUO-induced expression of inflammatory cytokines and extracellular matrix proteins was abrogated by DFO treatment. DFO inhibited the activation of the transforming growth factor-β1 (TGF-β1)-Smad3 pathway in UUO mice. UUO-induced NADPH oxidase activity and p22(phox) expression were attenuated by DFO. In the kidneys of UUO mice, divalent metal transporter 1, ferroportin, and ferritin expression was higher and transferrin receptor expression was lower than in sham-operated mice. Increased renal iron content was observed in UUO mice, which was reduced by DFO treatment. These results suggest that iron reduction by DFO prevents renal tubulointerstitial fibrosis by regulating TGF-β-Smad signaling, oxidative stress, and inflammatory responses.","ja":"Renal fibrosis plays an important role in the onset and progression of chronic kidney diseases (CKD). Although several mechanisms underlying renal fibrosis and candidate drugs for its treatment have been identified, the effect of iron chelator on renal fibrosis remains unclear. In the present study, we examined the effect of an iron chelator, deferoxamine (DFO), on renal fibrosis in mice with surgically induced unilateral ureter obstruction (UUO). Mice were divided into 4 groups: UUO with vehicle, UUO with DFO, sham with vehicle, and sham with DFO. One week after surgery, augmented renal tubulointerstitial fibrosis and the expression of collagen I, III, and IV increased in mice with UUO; these changes were suppressed by DFO treatment. Similarly, UUO-induced macrophage infiltration of renal interstitial tubules was reduced in UUO mice treated with DFO. UUO-induced expression of inflammatory cytokines and extracellular matrix proteins was abrogated by DFO treatment. DFO inhibited the activation of the transforming growth factor-β1 (TGF-β1)-Smad3 pathway in UUO mice. UUO-induced NADPH oxidase activity and p22(phox) expression were attenuated by DFO. In the kidneys of UUO mice, divalent metal transporter 1, ferroportin, and ferritin expression was higher and transferrin receptor expression was lower than in sham-operated mice. Increased renal iron content was observed in UUO mice, which was reduced by DFO treatment. These results suggest that iron reduction by DFO prevents renal tubulointerstitial fibrosis by regulating TGF-β-Smad signaling, oxidative stress, and inflammatory responses."},"publication_date":"2014-02-19","publication_name":{"en":"PLoS ONE","ja":"PLoS ONE"},"volume":"Vol.9","number":"No.2","starting_page":"e89355","ending_page":"e89355","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1371/journal.pone.0089355"],"issn":["1932-6203"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:51, {"insert":{"user_id":"B000337971","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/24489716","label":"url"},{"@id":"https://www.scopus.com/record/display.url?eid=2-s2.0-84900332178&origin=inward","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=275165","label":"url"}],"paper_title":{"en":"Nitrosonifedipine ameliorates the progression of type 2 diabetic nephropathy by exerting antioxidative effects","ja":"Nitrosonifedipine ameliorates the progression of type 2 diabetic nephropathy by exerting antioxidative effects"},"authors":{"en":[{"name":"Ishizawa Keisuke"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Yamano Noriko"},{"name":"Urushihara Maki"},{"name":"Sakurada Takumi"},{"name":"Imanishi Masaki"},{"name":"Fujii Shoko"},{"name":"Nuno Asami"},{"name":"Miyamoto Licht"},{"name":"Kihira Yoshitaka"},{"name":"Ikeda Yasumasa"},{"name":"Kagami Shoji"},{"name":"Kobori Hiroyuki"},{"name":"Tsuchiya Koichiro"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"石澤 啓介"},{"name":"石澤 有紀"},{"name":"山野 範子"},{"name":"漆原 真樹"},{"name":"Sakurada Takumi"},{"name":"今西 正樹"},{"name":"Fujii Shoko"},{"name":"Nuno Asami"},{"name":"宮本 理人"},{"name":"木平 孝高"},{"name":"池田 康将"},{"name":"香美 祥二"},{"name":"Kobori Hiroyuki"},{"name":"土屋 浩一郎"},{"name":"玉置 俊晃"}]},"description":{"en":"Diabetic nephropathy (DN) is the major cause of end-stage renal failure. Oxidative stress is implicated in the pathogenesis of DN. Nitrosonifedipine (NO-NIF) is a weak calcium channel blocker that is converted from nifedipine under light exposure. Recently, we reported that NO-NIF has potential as a novel antioxidant with radical scavenging abilities and has the capacity to treat vascular dysfunction by exerting an endothelial protective effect. In the present study, we extended these findings by evaluating the efficacy of NO-NIF against DN and by clarifying the mechanisms of its antioxidative effect. In a model of type 2 DN (established in KKAy mice), NO-NIF administration reduced albuminuria and proteinuria as well as glomerular expansion without affecting glucose metabolism or systolic blood pressure. NO-NIF also suppressed renal and systemic oxidative stress and decreased the expression of intercellular adhesion molecule (ICAM)-1, a marker of endothelial cell injury, in the glomeruli of the KKAy mice. Similarly, NO-NIF reduced albuminuria, oxidative stress, and ICAM-1 expression in endothelial nitric oxide synthase (eNOS) knockout mice. Moreover, NO-NIF suppressed urinary angiotensinogen (AGT) excretion and intrarenal AGT protein expression in proximal tubular cells in the KKAy mice. On the other hand, hyperglycemia-induced mitochondrial superoxide production was not attenuated by NO-NIF in cultured endothelial cells. These findings suggest that NO-NIF prevents the progression of type 2 DN associated with endothelial dysfunction through selective antioxidative effects.","ja":"Diabetic nephropathy (DN) is the major cause of end-stage renal failure. Oxidative stress is implicated in the pathogenesis of DN. Nitrosonifedipine (NO-NIF) is a weak calcium channel blocker that is converted from nifedipine under light exposure. Recently, we reported that NO-NIF has potential as a novel antioxidant with radical scavenging abilities and has the capacity to treat vascular dysfunction by exerting an endothelial protective effect. In the present study, we extended these findings by evaluating the efficacy of NO-NIF against DN and by clarifying the mechanisms of its antioxidative effect. In a model of type 2 DN (established in KKAy mice), NO-NIF administration reduced albuminuria and proteinuria as well as glomerular expansion without affecting glucose metabolism or systolic blood pressure. NO-NIF also suppressed renal and systemic oxidative stress and decreased the expression of intercellular adhesion molecule (ICAM)-1, a marker of endothelial cell injury, in the glomeruli of the KKAy mice. Similarly, NO-NIF reduced albuminuria, oxidative stress, and ICAM-1 expression in endothelial nitric oxide synthase (eNOS) knockout mice. Moreover, NO-NIF suppressed urinary angiotensinogen (AGT) excretion and intrarenal AGT protein expression in proximal tubular cells in the KKAy mice. On the other hand, hyperglycemia-induced mitochondrial superoxide production was not attenuated by NO-NIF in cultured endothelial cells. These findings suggest that NO-NIF prevents the progression of type 2 DN associated with endothelial dysfunction through selective antioxidative effects."},"publication_date":"2014-01-28","publication_name":{"en":"PLoS ONE","ja":"PLoS ONE"},"volume":"Vol.9","number":"No.1","starting_page":"e86335","ending_page":"e86335","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1371/journal.pone.0086335"],"issn":["1932-6203"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:52, {"insert":{"user_id":"B000337971","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/23389454","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=261038","label":"url"}],"paper_title":{"en":"Dietary iron restriction inhibits progression of diabetic nephropathy in db/db mice.","ja":"Dietary iron restriction inhibits progression of diabetic nephropathy in db/db mice."},"authors":{"en":[{"name":"Ikeda Yasumasa"},{"name":"Enomoto Hideaki"},{"name":"Tajima Soichiro"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Kihira Yoshitaka"},{"name":"Ishizawa Keisuke"},{"name":"Tomita Shuhei"},{"name":"Tsuchiya Koichiro"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"池田 康将"},{"name":"榎本 英明"},{"name":"Tajima Soichiro"},{"name":"石澤 有紀"},{"name":"木平 孝高"},{"name":"石澤 啓介"},{"name":"冨田 修平"},{"name":"土屋 浩一郎"},{"name":"玉置 俊晃"}]},"description":{"en":"Excess iron causes oxidative stress through hydroxyl-radical production via Fenton/Haber-Weiss reactions. Recently, body iron reduction has been found to ameliorate diabetes. In the present study, we examined the protective effect of dietary iron restriction against diabetic nephropathy in the db/db mouse model of diabetic nephropathy using db/m mice as controls. The db/db mice were divided into 2 groups and fed a normal diet (ND) or a low iron diet (LID). Increasing urinary albumin excretion was observed in the ND db/db mice, but this was suppressed in db/db mice with LID. Histologically, the db/db mice in the ND group had increased glomerular volume and mesangial area compared to the LID group. Augmented deposition of extracellular matrices was decreased in db/db mice with LID. In terms of oxidative stress, increased superoxide production observed in the kidneys of the ND db/db mice was diminished in the LID group. NADPH oxidase activity and renal expression of NADPH oxidase components p22(phox) and NOX4 were augmented in the ND group, and this was abolished by LID. There were no differences in expression of renal iron importers, transferrin receptor, or divalent metal transporter-1 between db/m mice and db/db mice. The level of ferroportin, an iron exporter, increased in the kidneys of the db/db mice. Urinary iron excretion was significantly higher in ND db/db mice and was reduced in the LID group. These findings suggest that dietary iron restriction exerts a preventive effect on the progression of diabetic nephropathy partly due to the reduction of oxidative stress.","ja":"Excess iron causes oxidative stress through hydroxyl-radical production via Fenton/Haber-Weiss reactions. Recently, body iron reduction has been found to ameliorate diabetes. In the present study, we examined the protective effect of dietary iron restriction against diabetic nephropathy in the db/db mouse model of diabetic nephropathy using db/m mice as controls. The db/db mice were divided into 2 groups and fed a normal diet (ND) or a low iron diet (LID). Increasing urinary albumin excretion was observed in the ND db/db mice, but this was suppressed in db/db mice with LID. Histologically, the db/db mice in the ND group had increased glomerular volume and mesangial area compared to the LID group. Augmented deposition of extracellular matrices was decreased in db/db mice with LID. In terms of oxidative stress, increased superoxide production observed in the kidneys of the ND db/db mice was diminished in the LID group. NADPH oxidase activity and renal expression of NADPH oxidase components p22(phox) and NOX4 were augmented in the ND group, and this was abolished by LID. There were no differences in expression of renal iron importers, transferrin receptor, or divalent metal transporter-1 between db/m mice and db/db mice. The level of ferroportin, an iron exporter, increased in the kidneys of the db/db mice. Urinary iron excretion was significantly higher in ND db/db mice and was reduced in the LID group. These findings suggest that dietary iron restriction exerts a preventive effect on the progression of diabetic nephropathy partly due to the reduction of oxidative stress."},"publication_date":"2013-02-06","publication_name":{"en":"American Journal of Physiology, Renal Physiology","ja":"American Journal of Physiology, Renal Physiology"},"volume":"Vol.304","number":"No.7","starting_page":"F1028","ending_page":"F1036","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1152/ajprenal.00473.2012"],"issn":["1522-1466"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:53, {"insert":{"user_id":"B000337971","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/113754","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/23364610","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=259318","label":"url"}],"paper_title":{"en":"Bovine milk-derived lactoferrin exerts proangiogenic effects in an Src-Akt-eNOS-dependent manner in response to ischemia","ja":"Bovine milk-derived lactoferrin exerts proangiogenic effects in an Src-Akt-eNOS-dependent manner in response to ischemia"},"authors":{"en":[{"name":"Ikeda Yasumasa"},{"name":"Tajima Soichiro"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Kihira Yoshitaka"},{"name":"Ishizawa Keisuke"},{"name":"Yoshida Sumiko"},{"name":"Aihara Ken-ichi"},{"name":"Tsuchiya Koichiro"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"池田 康将"},{"name":"Tajima Soichiro"},{"name":"石澤 有紀"},{"name":"木平 孝高"},{"name":"石澤 啓介"},{"name":"吉田 守美子"},{"name":"粟飯原 賢一"},{"name":"土屋 浩一郎"},{"name":"玉置 俊晃"}]},"description":{"en":"Lactoferrin (LF) exerts a variety of biological effects, including the promotion of angiogenesis by increasing the expression of angiogenesis-related genes and reducing blood pressure via a nitric oxide-dependent mechanism. In this study, we investigated the effects of LF on angiogenesis using C57BL/6J mice that received daily unilateral treatment with or without bovine milk-derived LF (bLF) after unilateral hindlimb surgery. The analysis of laser speckle blood flow showed that bLF treatment promoted blood flow recovery in response to ischemic hindlimb. The capillary density of ischemic adductor muscles and the phosphorylation of Src, Akt, and endothelial nitric oxide synthase (eNOS) were also significantly higher in bLF-treated mice than in vehicle-treated mice. Furthermore, bLF increased the phosphorylation levels of Src, Akt, and eNOS in in vitro experiments using human aortic endothelial cells. The action of bLF on eNOS phosphorylation was abolished by both LY294002, a phosphatidylinositol 3-kinase inhibitor, and 4-amino-5-(4-chlorophenyl)-7-(dimethylethyl)pyrazolo [3,4-d]pyrimidine (PP2), an Src inhibitor. Similarly, bLF-induced acceleration of tube formation, cell proliferation, and cell migration in human aortic endothelial cells were inhibited by LY294002 or PP2. Thus, bLF promotes vascular endothelial cell function via an Src Akt eNOS-dependent pathway, thereby contributing to revascularization in response to ischemia.","ja":"Lactoferrin (LF) exerts a variety of biological effects, including the promotion of angiogenesis by increasing the expression of angiogenesis-related genes and reducing blood pressure via a nitric oxide-dependent mechanism. In this study, we investigated the effects of LF on angiogenesis using C57BL/6J mice that received daily unilateral treatment with or without bovine milk-derived LF (bLF) after unilateral hindlimb surgery. The analysis of laser speckle blood flow showed that bLF treatment promoted blood flow recovery in response to ischemic hindlimb. The capillary density of ischemic adductor muscles and the phosphorylation of Src, Akt, and endothelial nitric oxide synthase (eNOS) were also significantly higher in bLF-treated mice than in vehicle-treated mice. Furthermore, bLF increased the phosphorylation levels of Src, Akt, and eNOS in in vitro experiments using human aortic endothelial cells. The action of bLF on eNOS phosphorylation was abolished by both LY294002, a phosphatidylinositol 3-kinase inhibitor, and 4-amino-5-(4-chlorophenyl)-7-(dimethylethyl)pyrazolo [3,4-d]pyrimidine (PP2), an Src inhibitor. Similarly, bLF-induced acceleration of tube formation, cell proliferation, and cell migration in human aortic endothelial cells were inhibited by LY294002 or PP2. Thus, bLF promotes vascular endothelial cell function via an Src Akt eNOS-dependent pathway, thereby contributing to revascularization in response to ischemia."},"publication_date":"2013-01","publication_name":{"en":"Journal of Cardiovascular Pharmacology","ja":"Journal of Cardiovascular Pharmacology"},"volume":"Vol.61","number":"No.5","starting_page":"423","ending_page":"429","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1097/FJC.0b013e318287d526"],"issn":["1533-4023"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:54, {"insert":{"user_id":"B000337971","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/23149861","label":"url"},{"@id":"https://www.scopus.com/record/display.url?eid=2-s2.0-84872316103&origin=inward","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=257964","label":"url"}],"paper_title":{"en":"Nitrosonifedipine ameliorates angiotensin II-induced vascular remodeling via antioxidative effects","ja":"Nitrosonifedipine ameliorates angiotensin II-induced vascular remodeling via antioxidative effects"},"authors":{"en":[{"name":"Sakurada Takumi"},{"name":"Ishizawa Keisuke"},{"name":"Imanishi Masaki"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Fujii Shoko"},{"name":"Tominaga Erika"},{"name":"Tsuneishi Teppei"},{"name":"Horinouchi Yuya"},{"name":"Kihira Yoshitaka"},{"name":"Ikeda Yasumasa"},{"name":"Tomita Shuhei"},{"name":"Aihara Ken-ichi"},{"name":"Minakuchi Kazuo"},{"name":"Tsuchiya Koichiro"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"Sakurada Takumi"},{"name":"石澤 啓介"},{"name":"今西 正樹"},{"name":"石澤 有紀"},{"name":"Fujii Shoko"},{"name":"Tominaga Erika"},{"name":"Tsuneishi Teppei"},{"name":"堀ノ内 裕也"},{"name":"木平 孝高"},{"name":"池田 康将"},{"name":"冨田 修平"},{"name":"粟飯原 賢一"},{"name":"水口 和生"},{"name":"土屋 浩一郎"},{"name":"玉置 俊晃"}]},"description":{"en":"Nifedipine is unstable under light and decomposes to a stable nitroso analog, nitrosonifedipine (NO-NIF). The ability of NO-NIF to block calcium channels is quite weak compared with that of nifedipine. Recently, we have demonstrated that NO-NIF reacts with unsaturated fatty acid leading to generate NO-NIF radical, which acquires radical scavenging activity. However, the effects of NO-NIF on the pathogenesis related with oxidative stress, such as atherosclerosis and hypertension, are unclear. In this study, we investigated the effects of NO-NIF on angiotensin II (Ang II)-induced vascular remodeling. Ang II-induced thickening and fibrosis of aorta were inhibited by NO-NIF in mice. NO-NIF decreased reactive oxygen species (ROS) in the aorta and urinary 8-hydroxy-20-deoxyguanosine. Ang II-stimulated mRNA expressions of p22(phox), CD68, F4/80, monocyte chemoattractant protein-1, and collagen I in the aorta were inhibited by NO-NIF. Moreover, NO-NIF inhibited Ang II-induced cell migration and proliferation of vascular smooth muscle cells (VSMCs). NO-NIF reduced Ang II-induced ROS to the control level detected by dihydroethidium staining and lucigenin chemiluminescence assay in VSMCs. NO-NIF suppressed phosphorylations of Akt and epidermal growth factor receptor induced by Ang II. However, NO-NIF had no effects on intracellular Ca(2+) increase and protein kinase C-δ phosphorylation induced by Ang II in VSMCs. The electron paramagnetic resonance spectra indicated the continuous generation of NO-NIF radical of reaction with cultured VSMCs. These findings suggest that NO-NIF improves Ang II-induced vascular remodeling via the attenuation of oxidative stress.","ja":"Nifedipine is unstable under light and decomposes to a stable nitroso analog, nitrosonifedipine (NO-NIF). The ability of NO-NIF to block calcium channels is quite weak compared with that of nifedipine. Recently, we have demonstrated that NO-NIF reacts with unsaturated fatty acid leading to generate NO-NIF radical, which acquires radical scavenging activity. However, the effects of NO-NIF on the pathogenesis related with oxidative stress, such as atherosclerosis and hypertension, are unclear. In this study, we investigated the effects of NO-NIF on angiotensin II (Ang II)-induced vascular remodeling. Ang II-induced thickening and fibrosis of aorta were inhibited by NO-NIF in mice. NO-NIF decreased reactive oxygen species (ROS) in the aorta and urinary 8-hydroxy-20-deoxyguanosine. Ang II-stimulated mRNA expressions of p22(phox), CD68, F4/80, monocyte chemoattractant protein-1, and collagen I in the aorta were inhibited by NO-NIF. Moreover, NO-NIF inhibited Ang II-induced cell migration and proliferation of vascular smooth muscle cells (VSMCs). NO-NIF reduced Ang II-induced ROS to the control level detected by dihydroethidium staining and lucigenin chemiluminescence assay in VSMCs. NO-NIF suppressed phosphorylations of Akt and epidermal growth factor receptor induced by Ang II. However, NO-NIF had no effects on intracellular Ca(2+) increase and protein kinase C-δ phosphorylation induced by Ang II in VSMCs. The electron paramagnetic resonance spectra indicated the continuous generation of NO-NIF radical of reaction with cultured VSMCs. These findings suggest that NO-NIF improves Ang II-induced vascular remodeling via the attenuation of oxidative stress."},"publication_date":"2013-01","publication_name":{"en":"Naunyn-Schmiedeberg's Archives of Pharmacology","ja":"Naunyn-Schmiedeberg's Archives of Pharmacology"},"volume":"Vol.386","number":"No.1","starting_page":"29","ending_page":"39","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1007/s00210-012-0810-7"],"issn":["1432-1912"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:55, {"insert":{"user_id":"B000337971","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/23052181","label":"url"},{"@id":"https://www.scopus.com/record/display.url?eid=2-s2.0-84867214872&origin=inward","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=256474","label":"url"}],"paper_title":{"en":"Angiotensin II receptor blocker improves tumor necrosis factor-α-induced cytotoxicity via antioxidative effect in human glomerular endothelial cells","ja":"Angiotensin II receptor blocker improves tumor necrosis factor-α-induced cytotoxicity via antioxidative effect in human glomerular endothelial cells"},"authors":{"en":[{"name":"Izawa-Ishizawa Yuki"},{"name":"Ishizawa Keisuke"},{"name":"Sakurada Takumi"},{"name":"Imanishi Masaki"},{"name":"Miyamoto Licht"},{"name":"Fujii Shoko"},{"name":"Taira Hironori"},{"name":"Kihira Yoshitaka"},{"name":"Ikeda Yasumasa"},{"name":"Hamano Shuichi"},{"name":"Tomita Shuhei"},{"name":"Tsuchiya Koichiro"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"石澤 有紀"},{"name":"石澤 啓介"},{"name":"Sakurada Takumi"},{"name":"今西 正樹"},{"name":"宮本 理人"},{"name":"Fujii Shoko"},{"name":"Taira Hironori"},{"name":"木平 孝高"},{"name":"池田 康将"},{"name":"濱野 修一"},{"name":"冨田 修平"},{"name":"土屋 浩一郎"},{"name":"玉置 俊晃"}]},"description":{"en":"Tumor necrosis factor-α (TNF-α) is known to involve the progression of renal dysfunction through its cytotoxicity and proinflammatory effects such as the induction of intercellular adhesion molecule (ICAM)-1 expression in vascular endothelial cells (ECs). Olmesartan, one of the angiotensin II type 1 receptor blockers (ARBs), has been reported to show protective effects on injured ECs by some causal factors of renal disorder other than angiotensin II. However, the effects of olmesartan on TNF-α-induced glomerular EC damage have not been investigated. In the present study, we investigated the effects of RNH-6270, an active metabolite of olmesartan, on TNF-α-induced human glomerular EC (HGEC) damage to clarify the renoprotective mechanisms of ARBs. Cultured HGECs were stimulated by TNF-α, and then cell viability and cytotoxicity were measured by MTT assay and lactate dehydrogenase release assay, respectively. TNF-α-induced oxidative stress was estimated by dihydroethidium assay and lucigenin chemiluminescence assay. ICAM-1 expression and the phosphorylations of mitogen-activated protein kinases were measured using Western blotting assay. RNH-6270 suppressed cell death and the increase in ICAM-1 expression induced by TNF-α via the inhibition of reactive oxygen species in HGECs. Our findings suggested that olmesartan might have protective effects against TNF-α-induced glomerular EC dysfunction.","ja":"Tumor necrosis factor-α (TNF-α) is known to involve the progression of renal dysfunction through its cytotoxicity and proinflammatory effects such as the induction of intercellular adhesion molecule (ICAM)-1 expression in vascular endothelial cells (ECs). Olmesartan, one of the angiotensin II type 1 receptor blockers (ARBs), has been reported to show protective effects on injured ECs by some causal factors of renal disorder other than angiotensin II. However, the effects of olmesartan on TNF-α-induced glomerular EC damage have not been investigated. In the present study, we investigated the effects of RNH-6270, an active metabolite of olmesartan, on TNF-α-induced human glomerular EC (HGEC) damage to clarify the renoprotective mechanisms of ARBs. Cultured HGECs were stimulated by TNF-α, and then cell viability and cytotoxicity were measured by MTT assay and lactate dehydrogenase release assay, respectively. TNF-α-induced oxidative stress was estimated by dihydroethidium assay and lucigenin chemiluminescence assay. ICAM-1 expression and the phosphorylations of mitogen-activated protein kinases were measured using Western blotting assay. RNH-6270 suppressed cell death and the increase in ICAM-1 expression induced by TNF-α via the inhibition of reactive oxygen species in HGECs. Our findings suggested that olmesartan might have protective effects against TNF-α-induced glomerular EC dysfunction."},"publication_date":"2012-12","publication_name":{"en":"Pharmacology","ja":"Pharmacology"},"volume":"Vol.90","number":"No.5-6","starting_page":"324","ending_page":"331","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1159/000343244"],"issn":["1423-0313"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:56, {"insert":{"user_id":"B000337971","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/22904320","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=253941","label":"url"}],"paper_title":{"en":"Heparin cofactor II, a serine protease inhibitor, promotes angiogenesis via activation of the AMP-activated protein kinase-endothelial nitric-oxide synthase signaling pathway","ja":"Heparin cofactor II, a serine protease inhibitor, promotes angiogenesis via activation of the AMP-activated protein kinase-endothelial nitric-oxide synthase signaling pathway"},"authors":{"en":[{"name":"Ikeda Yasumasa"},{"name":"Aihara Ken-ichi"},{"name":"Yoshida Sumiko"},{"name":"Iwase Takashi"},{"name":"Tajima Soichiro"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Kihira Yoshitaka"},{"name":"Ishizawa Keisuke"},{"name":"Tomita Shuhei"},{"name":"Tsuchiya Koichiro"},{"name":"Sata Masataka"},{"name":"Akaike Masashi"},{"name":"Kato Shigeaki"},{"name":"Matsumoto Toshio"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"池田 康将"},{"name":"粟飯原 賢一"},{"name":"吉田 守美子"},{"name":"岩瀬 俊"},{"name":"Tajima Soichiro"},{"name":"石澤 有紀"},{"name":"木平 孝高"},{"name":"石澤 啓介"},{"name":"冨田 修平"},{"name":"土屋 浩一郎"},{"name":"佐田 政隆"},{"name":"赤池 雅史"},{"name":"Kato Shigeaki"},{"name":"松本 俊夫"},{"name":"玉置 俊晃"}]},"description":{"en":"We previously clarified that heparin cofactor II (HCII), a serine proteinase inhibitor, exerts various protective actions on cardiovascular diseases in both experimental and clinical studies. In the present study, we aimed to clarify whether HCII participates in the regulation of angiogenesis. Male heterozygous HCII-deficient (HCII(+/-)) mice and male littermate wild-type (HCII(+/+)) mice at the age of 12-16 weeks were subjected to unilateral hindlimb ligation surgery. Laser speckle blood flow analysis showed that blood flow recovery in response to hindlimb ischemia was delayed in HCII(+/-) mice compared with that in HCII(+/+) mice. Capillary number, arteriole number, and endothelial nitric-oxide synthase (eNOS), AMP-activated protein kinase (AMPK), and liver kinase B1 (LKB1) phosphorylation in ischemic muscles were decreased in HCII(+/-) mice. Human purified HCII (h-HCII) administration almost restored blood flow recovery, capillary density, and arteriole number as well as phosphorylation levels of eNOS, AMPK, and LKB1 in ischemic muscles of HCII(+/-) mice. Although treatment with h-HCII increased phosphorylation levels of eNOS, AMPK, and LKB1 in human aortic endothelial cells (HAECs), the h-HCII-induced eNOS phosphorylation was abolished by compound C, an AMPK inhibitor, and by AMPK siRNA. In a similar fashion, tube formation, proliferation, and migration of HAECs were also promoted by h-HCII treatment and were abrogated by pretreatment with compound C. HCII potentiates the activation of vascular endothelial cells and the promotion of angiogenesis in response to hindlimb ischemia via an AMPK-eNOS signaling pathway. These findings suggest that HCII is a novel therapeutic target for treatment of patients with peripheral circulation insufficiency.","ja":"We previously clarified that heparin cofactor II (HCII), a serine proteinase inhibitor, exerts various protective actions on cardiovascular diseases in both experimental and clinical studies. In the present study, we aimed to clarify whether HCII participates in the regulation of angiogenesis. Male heterozygous HCII-deficient (HCII(+/-)) mice and male littermate wild-type (HCII(+/+)) mice at the age of 12-16 weeks were subjected to unilateral hindlimb ligation surgery. Laser speckle blood flow analysis showed that blood flow recovery in response to hindlimb ischemia was delayed in HCII(+/-) mice compared with that in HCII(+/+) mice. Capillary number, arteriole number, and endothelial nitric-oxide synthase (eNOS), AMP-activated protein kinase (AMPK), and liver kinase B1 (LKB1) phosphorylation in ischemic muscles were decreased in HCII(+/-) mice. Human purified HCII (h-HCII) administration almost restored blood flow recovery, capillary density, and arteriole number as well as phosphorylation levels of eNOS, AMPK, and LKB1 in ischemic muscles of HCII(+/-) mice. Although treatment with h-HCII increased phosphorylation levels of eNOS, AMPK, and LKB1 in human aortic endothelial cells (HAECs), the h-HCII-induced eNOS phosphorylation was abolished by compound C, an AMPK inhibitor, and by AMPK siRNA. In a similar fashion, tube formation, proliferation, and migration of HAECs were also promoted by h-HCII treatment and were abrogated by pretreatment with compound C. HCII potentiates the activation of vascular endothelial cells and the promotion of angiogenesis in response to hindlimb ischemia via an AMPK-eNOS signaling pathway. These findings suggest that HCII is a novel therapeutic target for treatment of patients with peripheral circulation insufficiency."},"publication_date":"2012-10","publication_name":{"en":"The Journal of Biological Chemistry","ja":"The Journal of Biological Chemistry"},"volume":"Vol.287","number":"No.41","starting_page":"34256","ending_page":"34263","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1074/jbc.M112.353532"],"issn":["1083-351X"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:57, {"insert":{"user_id":"B000337971","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"http://ci.nii.ac.jp/naid/40019353020/","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/22792339","label":"url"},{"@id":"https://www.scopus.com/record/display.url?eid=2-s2.0-84863827034&origin=inward","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=248250","label":"url"}],"paper_title":{"en":"Estrogen regulates hepcidin expression via GPR30-BMP6-dependent signaling in hepatocytes","ja":"Estrogen regulates hepcidin expression via GPR30-BMP6-dependent signaling in hepatocytes"},"authors":{"en":[{"name":"Ikeda Yasumasa"},{"name":"Tajima Soichiro"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Kihira Yoshitaka"},{"name":"Ishizawa Keisuke"},{"name":"Tomita Shuhei"},{"name":"Tsuchiya Koichiro"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"池田 康将"},{"name":"Tajima Soichiro"},{"name":"石澤 有紀"},{"name":"木平 孝高"},{"name":"石澤 啓介"},{"name":"冨田 修平"},{"name":"土屋 浩一郎"},{"name":"玉置 俊晃"}]},"description":{"en":"Hepcidin, a liver-derived iron regulatory protein, plays a crucial role in iron metabolism. It is known that gender differences exist with respect to iron storage in the body; however, the effects of sex steroid hormones on iron metabolism are not completely understood. We focused on the effects of the female sex hormone estrogen on hepcidin expression. First, ovariectomized (OVX) and sham-operated mice were employed to investigate the effects of estrogen on hepcidin expression in an in vivo study. Hepcidin expression was decreased in the livers of OVX mice compared to the sham-operated mice. In OVX mice, bone morphologic protein-6 (BMP6), a regulator of hepcidin, was also found to be downregulated in the liver, whereas ferroportin (FPN), an iron export protein, was upregulated in the duodenum. Both serum and liver iron concentrations were elevated in OVX mice relative to their concentrations in sham-operated mice. In in vitro studies, 17β-estradiol (E(2)) increased the mRNA expression of hepcidin in HepG2 cells in a concentration-dependent manner. E(2)-induced hepatic hepcidin upregulation was not inhibited by ICI 182720, an inhibitor of the estrogen receptor; instead, hepcidin expression was increased by ICI 182720. E(2) and ICI 182720 exhibit agonist actions with G-protein coupled receptor 30 (GPR30), the 7-transmembrane estrogen receptor. G1, a GPR30 agonist, upregulated hepcidin expression, and GPR30 siRNA treatment abolished E(2)-induced hepcidin expression. BMP6 expression induced by E(2) was abolished by GPR30 silencing. Finally, both E(2) and G1 supplementation restored reduced hepatic hepcidin and BMP6 expression and reversed the augmentation of duodenal FPN expression in the OVX mice. In contrast, serum hepcidin was elevated in OVX mice, which was reversed in these mice with E(2) and G1. Thus, estrogen is involved in hepcidin expression via a GPR30-BMP6-dependent mechanism, providing new insight into the role of estrogen in iron metabolism.","ja":"Hepcidin, a liver-derived iron regulatory protein, plays a crucial role in iron metabolism. It is known that gender differences exist with respect to iron storage in the body; however, the effects of sex steroid hormones on iron metabolism are not completely understood. We focused on the effects of the female sex hormone estrogen on hepcidin expression. First, ovariectomized (OVX) and sham-operated mice were employed to investigate the effects of estrogen on hepcidin expression in an in vivo study. Hepcidin expression was decreased in the livers of OVX mice compared to the sham-operated mice. In OVX mice, bone morphologic protein-6 (BMP6), a regulator of hepcidin, was also found to be downregulated in the liver, whereas ferroportin (FPN), an iron export protein, was upregulated in the duodenum. Both serum and liver iron concentrations were elevated in OVX mice relative to their concentrations in sham-operated mice. In in vitro studies, 17β-estradiol (E(2)) increased the mRNA expression of hepcidin in HepG2 cells in a concentration-dependent manner. E(2)-induced hepatic hepcidin upregulation was not inhibited by ICI 182720, an inhibitor of the estrogen receptor; instead, hepcidin expression was increased by ICI 182720. E(2) and ICI 182720 exhibit agonist actions with G-protein coupled receptor 30 (GPR30), the 7-transmembrane estrogen receptor. G1, a GPR30 agonist, upregulated hepcidin expression, and GPR30 siRNA treatment abolished E(2)-induced hepcidin expression. BMP6 expression induced by E(2) was abolished by GPR30 silencing. Finally, both E(2) and G1 supplementation restored reduced hepatic hepcidin and BMP6 expression and reversed the augmentation of duodenal FPN expression in the OVX mice. In contrast, serum hepcidin was elevated in OVX mice, which was reversed in these mice with E(2) and G1. Thus, estrogen is involved in hepcidin expression via a GPR30-BMP6-dependent mechanism, providing new insight into the role of estrogen in iron metabolism."},"publication_date":"2012-07-11","publication_name":{"en":"PLoS ONE","ja":"PLoS ONE"},"volume":"Vol.7","number":"No.7","starting_page":"e40465","ending_page":"e40465","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1371/journal.pone.0040465"],"issn":["1932-6203"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:58, {"insert":{"user_id":"B000337971","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/21917632","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=243340","label":"url"}],"paper_title":{"en":"Iron reduction by deferoxamine leads to amelioration of adiposity via the regulation of oxidative stress and inflammation in obese and type 2 diabetes KKAy mice.","ja":"Iron reduction by deferoxamine leads to amelioration of adiposity via the regulation of oxidative stress and inflammation in obese and type 2 diabetes KKAy mice."},"authors":{"en":[{"name":"Tajima Soichiro"},{"name":"Ikeda Yasumasa"},{"name":"Sawada Kaori"},{"name":"Yamano Noriko"},{"name":"Horinouchi Yuya"},{"name":"Kihira Yoshitaka"},{"name":"Ishizawa Keisuke"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Kawazoe Kazuyoshi"},{"name":"Tomita Shuhei"},{"name":"Minakuchi Kazuo"},{"name":"Tsuchiya Koichiro"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"Tajima Soichiro"},{"name":"池田 康将"},{"name":"澤田 香織"},{"name":"山野 範子"},{"name":"堀ノ内 裕也"},{"name":"木平 孝高"},{"name":"石澤 啓介"},{"name":"石澤 有紀"},{"name":"川添 和義"},{"name":"冨田 修平"},{"name":"水口 和生"},{"name":"土屋 浩一郎"},{"name":"玉置 俊晃"}]},"description":{"en":"Iron is an essential trace metal for most organisms. However, excess iron causes oxidative stress through production of highly toxic hydroxyl radicals via the Fenton/Haber-Weiss reaction. Iron storage in the body is reported to be associated with fat accumulation and type 2 diabetes mellitus. We investigated the role of iron in adiposity by using KKAy mice and obese and diabetic model mice. Eight-week-old KKAy mice were divided into two groups and treated with deferoxamine (DFO), an iron chelator agent, or a vehicle for 2 wk. DFO treatment diminished fat iron concentration and serum ferritin levels in KKAy mice. Fat weight and adipocyte size were reduced significantly in DFO-treated mice compared with vehicle-treated mice. Macrophage infiltration into fat was also decreased in DFO-treated mice compared with vehicle-treated mice. Superoxide production and NADPH oxidase activity in fat, as well as urinary 8-hydroxy-2'-deoxyguanosine excretion, were decreased in KKAy mice after DFO treatment while p22(phox) expression in adipose tissue was diminished in such mice. Ferritin expression in the fat of DFO-treated KKAy mice was decreased. In addition, F4/80-positive cells also presented through both p22(phox) and ferritin expression. The mRNA expression levels of inflammatory cytokines were also reduced in fat tissue of DFO-treated mice. These findings suggest that reduction of iron levels ameliorates adipocyte hypertrophy via suppression of oxidative stress, inflammatory cytokines, and macrophage infiltration, thereby breaking a vicious cycle in obesity.","ja":"Iron is an essential trace metal for most organisms. However, excess iron causes oxidative stress through production of highly toxic hydroxyl radicals via the Fenton/Haber-Weiss reaction. Iron storage in the body is reported to be associated with fat accumulation and type 2 diabetes mellitus. We investigated the role of iron in adiposity by using KKAy mice and obese and diabetic model mice. Eight-week-old KKAy mice were divided into two groups and treated with deferoxamine (DFO), an iron chelator agent, or a vehicle for 2 wk. DFO treatment diminished fat iron concentration and serum ferritin levels in KKAy mice. Fat weight and adipocyte size were reduced significantly in DFO-treated mice compared with vehicle-treated mice. Macrophage infiltration into fat was also decreased in DFO-treated mice compared with vehicle-treated mice. Superoxide production and NADPH oxidase activity in fat, as well as urinary 8-hydroxy-2'-deoxyguanosine excretion, were decreased in KKAy mice after DFO treatment while p22(phox) expression in adipose tissue was diminished in such mice. Ferritin expression in the fat of DFO-treated KKAy mice was decreased. In addition, F4/80-positive cells also presented through both p22(phox) and ferritin expression. The mRNA expression levels of inflammatory cytokines were also reduced in fat tissue of DFO-treated mice. These findings suggest that reduction of iron levels ameliorates adipocyte hypertrophy via suppression of oxidative stress, inflammatory cytokines, and macrophage infiltration, thereby breaking a vicious cycle in obesity."},"publication_date":"2012-01","publication_name":{"en":"American Journal of Physiology, Endocrinology and Metabolism","ja":"American Journal of Physiology, Endocrinology and Metabolism"},"volume":"Vol.302","number":"No.1","starting_page":"E77","ending_page":"86","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1152/ajpendo.00033.2011"],"issn":["1522-1555"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:59, {"insert":{"user_id":"B000337971","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/21810481","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=241773","label":"url"}],"paper_title":{"en":"Basic fibroblast growth factor regulates glucose metabolism through glucose transporter 1 induced by hypoxia-inducible factor-1α in adipocytes","ja":"Basic fibroblast growth factor regulates glucose metabolism through glucose transporter 1 induced by hypoxia-inducible factor-1α in adipocytes"},"authors":{"en":[{"name":"Kihira Yoshitaka"},{"name":"Yamano Noriko"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Ishizawa Keisuke"},{"name":"Ikeda Yasumasa"},{"name":"Tsuchiya Koichiro"},{"name":"Tamaki Toshiaki"},{"name":"Tomita Shuhei"}],"ja":[{"name":"木平 孝高"},{"name":"山野 範子"},{"name":"石澤 有紀"},{"name":"石澤 啓介"},{"name":"池田 康将"},{"name":"土屋 浩一郎"},{"name":"玉置 俊晃"},{"name":"冨田 修平"}]},"description":{"en":"Hypoxia-inducible factor-1 (HIF-1), which is a transcription factor that enhances glycolysis in cells in response to hypoxia, is induced in hypertrophied adipocytes in obesity. Recent studies have shown that growth factors are able to induce HIF-1 by mechanisms independent of hypoxia. Since basic fibroblast growth factor (bFGF), an angiogenic factor, is concentrated in expanding adipose tissue, the possible effects of bFGF on regulation of HIF-1 in adipocytes were investigated. Treatment of differentiated 3T3-L1 adipocytes with bFGF induced HIF-1. Concomitantly, glucose transporter 1 (GLUT1), which is a target gene of HIF-1, was induced at both mRNA and protein levels and was translocated to the plasma membrane. A chromatin immunoprecipitation assay and an RNA interference study indicated that bFGF-induced HIF-1 directly upregulates GLUT1. In addition, it was observed that bFGF increases lactate production of adipocytes. This result indicates that bFGF reprograms the metabolism toward glycolysis. Intraperitoneal injection of bFGF into mice upregulated HIF-1 and GLUT1 in adipose tissues, suggesting that bFGF regulates the metabolism of adipocytes via HIF-1-GLUT1 regulation in vivo. We also found that bFGF inhibits insulin-induced phosphorylation of insulin receptor substrate-1 and Akt, suggesting that bFGF attenuates the insulin signal in adipocytes. Taken together, the findings suggest that bFGF has a harmful effect on the development of type 2 diabetes through metabolism reprogramming and attenuation of the insulin signal.","ja":"Hypoxia-inducible factor-1 (HIF-1), which is a transcription factor that enhances glycolysis in cells in response to hypoxia, is induced in hypertrophied adipocytes in obesity. Recent studies have shown that growth factors are able to induce HIF-1 by mechanisms independent of hypoxia. Since basic fibroblast growth factor (bFGF), an angiogenic factor, is concentrated in expanding adipose tissue, the possible effects of bFGF on regulation of HIF-1 in adipocytes were investigated. Treatment of differentiated 3T3-L1 adipocytes with bFGF induced HIF-1. Concomitantly, glucose transporter 1 (GLUT1), which is a target gene of HIF-1, was induced at both mRNA and protein levels and was translocated to the plasma membrane. A chromatin immunoprecipitation assay and an RNA interference study indicated that bFGF-induced HIF-1 directly upregulates GLUT1. In addition, it was observed that bFGF increases lactate production of adipocytes. This result indicates that bFGF reprograms the metabolism toward glycolysis. Intraperitoneal injection of bFGF into mice upregulated HIF-1 and GLUT1 in adipose tissues, suggesting that bFGF regulates the metabolism of adipocytes via HIF-1-GLUT1 regulation in vivo. We also found that bFGF inhibits insulin-induced phosphorylation of insulin receptor substrate-1 and Akt, suggesting that bFGF attenuates the insulin signal in adipocytes. Taken together, the findings suggest that bFGF has a harmful effect on the development of type 2 diabetes through metabolism reprogramming and attenuation of the insulin signal."},"publication_date":"2011-11","publication_name":{"en":"The International Journal of Biochemistry & Cell Biology","ja":"The International Journal of Biochemistry & Cell Biology"},"volume":"Vol.43","number":"No.11","starting_page":"1602","ending_page":"1611","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1016/j.biocel.2011.07.009"],"issn":["1878-5875"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:60, {"insert":{"user_id":"B000337971","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/19812233","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=194522","label":"url"}],"paper_title":{"en":"Angiotensin II receptor blocker attenuates PDGF-induced mesangial cell migration in a receptor-independent manner","ja":"Angiotensin II receptor blocker attenuates PDGF-induced mesangial cell migration in a receptor-independent manner"},"authors":{"en":[{"name":"Ishizawa Keisuke"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Dorjsuren Narantungalag"},{"name":"Miki Erika"},{"name":"Kihira Yoshitaka"},{"name":"Ikeda Yasumasa"},{"name":"Hamano Shuichi"},{"name":"Kawazoe Kazuyoshi"},{"name":"Minakuchi Kazuo"},{"name":"Tomita Shuhei"},{"name":"Tsuchiya Koichiro"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"石澤 啓介"},{"name":"石澤 有紀"},{"name":"Dorjsuren Narantungalag"},{"name":"Miki Erika"},{"name":"木平 孝高"},{"name":"池田 康将"},{"name":"濱野 修一"},{"name":"川添 和義"},{"name":"水口 和生"},{"name":"冨田 修平"},{"name":"土屋 浩一郎"},{"name":"玉置 俊晃"}]},"description":{"en":"Clinical studies have shown that angiotensin II (Ang II) type 1 (AT1) receptor blockers (ARBs) are able to provide renoprotection independent of their blood pressure lowering effects. ARBs also are reported to suppress oxidative stress, inflammation and certain other cellular responses in a receptor-independent manner. We investigated the effects of an ARB, olmesartan, on the cell migration induced by platelet-derived growth factor (PDGF), a major mitogen involved in the pathogenesis of glomerulonephritis in rat mesangial cells (RMCs). Cell migration was determined by a modified Boyden chamber assay. The intracellular signalling pathway was examined by western blotting. AT1 receptor expression was knocked down by small interfering RNAs. The intracellular reactive oxygen species (ROS) was measured by using a fluorescent probe. The O(2)(.-) scavenging activities were studied by the electron paramagnetic resonance-spin trapping method. PDGF-induced cell migration was inhibited by olmesartan in AT1 receptor knockdown RMCs. Olmesartan attenuated big mitogen-activated protein (MAP) kinase 1 (BMK1) and Src activation by PDGF in AT1 receptor knockdown RMCs. PDGF-induced BMK1 activation was suppressed by the Src family tyrosine kinase inhibitors, indicating that Src exists upstream of BMK1. The NADPH oxidase inhibitors inhibited not only PDGF-induced BMK1 and Src activation but also RMC migration. The elevation in ROS generation induced by PDGF was decreased by olmesartan. Olmesartan displayed neither directly ROS scavenging activity nor the inhibition of ROS-mediated intracellular signalling in RMCs. Olmesartan attenuates ROS generation by PDGF, leading to the subsequent inhibition of Src/ BMK1/migration in an AT1 receptor-independent manner in RMCs.","ja":"Clinical studies have shown that angiotensin II (Ang II) type 1 (AT1) receptor blockers (ARBs) are able to provide renoprotection independent of their blood pressure lowering effects. ARBs also are reported to suppress oxidative stress, inflammation and certain other cellular responses in a receptor-independent manner. We investigated the effects of an ARB, olmesartan, on the cell migration induced by platelet-derived growth factor (PDGF), a major mitogen involved in the pathogenesis of glomerulonephritis in rat mesangial cells (RMCs). Cell migration was determined by a modified Boyden chamber assay. The intracellular signalling pathway was examined by western blotting. AT1 receptor expression was knocked down by small interfering RNAs. The intracellular reactive oxygen species (ROS) was measured by using a fluorescent probe. The O(2)(.-) scavenging activities were studied by the electron paramagnetic resonance-spin trapping method. PDGF-induced cell migration was inhibited by olmesartan in AT1 receptor knockdown RMCs. Olmesartan attenuated big mitogen-activated protein (MAP) kinase 1 (BMK1) and Src activation by PDGF in AT1 receptor knockdown RMCs. PDGF-induced BMK1 activation was suppressed by the Src family tyrosine kinase inhibitors, indicating that Src exists upstream of BMK1. The NADPH oxidase inhibitors inhibited not only PDGF-induced BMK1 and Src activation but also RMC migration. The elevation in ROS generation induced by PDGF was decreased by olmesartan. Olmesartan displayed neither directly ROS scavenging activity nor the inhibition of ROS-mediated intracellular signalling in RMCs. Olmesartan attenuates ROS generation by PDGF, leading to the subsequent inhibition of Src/ BMK1/migration in an AT1 receptor-independent manner in RMCs."},"publication_date":"2010-02","publication_name":{"en":"Nephrology, Dialysis, Transplantation","ja":"Nephrology, Dialysis, Transplantation"},"volume":"Vol.25","number":"No.2","starting_page":"364","ending_page":"372","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1093/ndt/gfp520"],"issn":["1460-2385"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:61, {"insert":{"user_id":"B000337971","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/20007912","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=202019","label":"url"}],"paper_title":{"en":"Role of Hypoxia-Inducible Factor 1α in T Cells as a Negative Regulator in Development of Vascular Remodeling","ja":"Role of Hypoxia-Inducible Factor 1α in T Cells as a Negative Regulator in Development of Vascular Remodeling"},"authors":{"en":[{"name":"Kurobe Hirotsugu"},{"name":"Urata Masahisa"},{"name":"Ueno Masaki"},{"name":"Ueki Masaaki"},{"name":"Ono Shiro"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Fukuhara Yayoi"},{"name":"Lei Yu"},{"name":"Ripen Mat Adiratna"},{"name":"Kanbara Tamotsu"},{"name":"Aihara Ken-ichi"},{"name":"Ishizawa Keisuke"},{"name":"Akaike Masashi"},{"name":"Gonzalez J. Frank"},{"name":"Tamaki Toshiaki"},{"name":"Takahama Yousuke"},{"name":"Yoshizumi Masanori"},{"name":"Kitagawa Tetsuya"},{"name":"Tomita Shuhei"}],"ja":[{"name":"黒部 裕嗣"},{"name":"Urata Masahisa"},{"name":"Ueno Masaki"},{"name":"Ueki Masaaki"},{"name":"Ono Shiro"},{"name":"石澤 有紀"},{"name":"Fukuhara Yayoi"},{"name":"Lei Yu"},{"name":"Ripen Mat Adiratna"},{"name":"神原 保"},{"name":"粟飯原 賢一"},{"name":"石澤 啓介"},{"name":"赤池 雅史"},{"name":"Gonzalez J. Frank"},{"name":"玉置 俊晃"},{"name":"高浜 洋介"},{"name":"吉栖 正典"},{"name":"北川 哲也"},{"name":"冨田 修平"}]},"description":{"en":"Recent studies have shown that the cellular immune response in the development of vascular remodeling modulates the resulting pathological alterations. We show that hypoxia-inducible factor 1 (Hif-1) (specifically expressed in T cells) is involved in the immune response to vascular remodeling that accompanies arteriosclerosis. To study the role of T cells in the development of vascular remodeling, femoral arterial injury induced by an external vascular polyethylene cuff was examined in mice lacking Hif-1 (specifically in T cells). We found that cuff placement caused prominent neointimal hyperplasia of the femoral artery in Hif-1- (T-cell)-deficient mice compared with that in control mice and that infiltration of inflammatory cells at the adventitia was markedly increased in the mutant mice. Studies to clarify the mechanism of augmented vascular remodeling in the mutant mice showed enhanced production of cytokines by activated T cells and augmented antibody production in response to a T-dependent antigen in the mutant mice. The results of this study revealed that Hif-1alpha in T cells plays a crucial role in vascular inflammation and remodeling in response to cuff injury as a negative regulator of T cell-mediated immune response. Potential new therapeutic strategies that target Hif-1alpha are described.","ja":"Recent studies have shown that the cellular immune response in the development of vascular remodeling modulates the resulting pathological alterations. We show that hypoxia-inducible factor 1 (Hif-1) (specifically expressed in T cells) is involved in the immune response to vascular remodeling that accompanies arteriosclerosis. To study the role of T cells in the development of vascular remodeling, femoral arterial injury induced by an external vascular polyethylene cuff was examined in mice lacking Hif-1 (specifically in T cells). We found that cuff placement caused prominent neointimal hyperplasia of the femoral artery in Hif-1- (T-cell)-deficient mice compared with that in control mice and that infiltration of inflammatory cells at the adventitia was markedly increased in the mutant mice. Studies to clarify the mechanism of augmented vascular remodeling in the mutant mice showed enhanced production of cytokines by activated T cells and augmented antibody production in response to a T-dependent antigen in the mutant mice. The results of this study revealed that Hif-1alpha in T cells plays a crucial role in vascular inflammation and remodeling in response to cuff injury as a negative regulator of T cell-mediated immune response. Potential new therapeutic strategies that target Hif-1alpha are described."},"publication_date":"2010-02","publication_name":{"en":"Arteriosclerosis, Thrombosis, and Vascular Biology","ja":"Arteriosclerosis, Thrombosis, and Vascular Biology"},"volume":"Vol.30","number":"No.2","starting_page":"210","ending_page":"217","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1161/ATVBAHA.109.192666"],"issn":["1524-4636"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:62, {"insert":{"user_id":"B000337971","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/19460854","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=193058","label":"url"}],"paper_title":{"en":"Inhibitory effects of adiponectin on platelet-derived growth factor-induced mesangial cell migration","ja":"Inhibitory effects of adiponectin on platelet-derived growth factor-induced mesangial cell migration"},"authors":{"en":[{"name":"Ishizawa Keisuke"},{"name":"Dorjsuren Narantungalag"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Sugimoto Rika"},{"name":"Ikeda Yasumasa"},{"name":"Kihira Yoshitaka"},{"name":"Kawazoe Kazuyoshi"},{"name":"Tomita Shuhei"},{"name":"Tsuchiya Koichiro"},{"name":"Minakuchi Kazuo"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"石澤 啓介"},{"name":"Dorjsuren Narantungalag"},{"name":"石澤 有紀"},{"name":"Sugimoto Rika"},{"name":"池田 康将"},{"name":"木平 孝高"},{"name":"川添 和義"},{"name":"冨田 修平"},{"name":"土屋 浩一郎"},{"name":"水口 和生"},{"name":"玉置 俊晃"}]},"description":{"en":"Adiponectin, an adipocyte-derived hormone, has been involved in metabolic syndrome, a known risk factor for the development of chronic kidney disease (CKD). Recent studies have demonstrated that plasma adiponectin levels are elevated when kidney function declines in patients with CKD. Excessive mesangial cell (MC) turnover is one of the important features of CKD. The aim of the present study is to elucidate the effects of adiponectin on platelet-derived growth factor (PDGF)-induced cell migration and intracellular signaling pathways, in cultured rat MCs (RMCs). PDGF-induced RMC migration was significantly inhibited by the pretreatment of adiponectin. Adiponectin alone had no effect on RMC migration. Big mitogen-activated protein (MAP) kinase 1 (BMK1), p38 MAP kinase, and Akt were activated by PDGF stimulation in a time- and concentration-dependent manner in RMC. Adiponectin alone did not affect BMK1, p38 MAP kinase, and Akt phosphorylations in RMC. PDGF-induced BMK1 and p38 MAP kinase phosphorylations were significantly attenuated by the pretreatment of adiponectin in RMCs. On the other hand, the phosphorylation of Akt by PDGF was not diminished by the pretreatment of adiponectin. Adiponectin had no effects on PDGF-receptor autophosphorylation by PDGF. We also confirmed that PDGF-induced RMC migration was significantly suppressed by siBMK1 transfection or SB203580, a p38 MAP kinase inhibitor. From these findings, it is implied that the elevated plasma adiponectin levels in patients with CKD might play a compensatory role aimed at counteracting renal dysfunction related to MC disorders.","ja":"Adiponectin, an adipocyte-derived hormone, has been involved in metabolic syndrome, a known risk factor for the development of chronic kidney disease (CKD). Recent studies have demonstrated that plasma adiponectin levels are elevated when kidney function declines in patients with CKD. Excessive mesangial cell (MC) turnover is one of the important features of CKD. The aim of the present study is to elucidate the effects of adiponectin on platelet-derived growth factor (PDGF)-induced cell migration and intracellular signaling pathways, in cultured rat MCs (RMCs). PDGF-induced RMC migration was significantly inhibited by the pretreatment of adiponectin. Adiponectin alone had no effect on RMC migration. Big mitogen-activated protein (MAP) kinase 1 (BMK1), p38 MAP kinase, and Akt were activated by PDGF stimulation in a time- and concentration-dependent manner in RMC. Adiponectin alone did not affect BMK1, p38 MAP kinase, and Akt phosphorylations in RMC. PDGF-induced BMK1 and p38 MAP kinase phosphorylations were significantly attenuated by the pretreatment of adiponectin in RMCs. On the other hand, the phosphorylation of Akt by PDGF was not diminished by the pretreatment of adiponectin. Adiponectin had no effects on PDGF-receptor autophosphorylation by PDGF. We also confirmed that PDGF-induced RMC migration was significantly suppressed by siBMK1 transfection or SB203580, a p38 MAP kinase inhibitor. From these findings, it is implied that the elevated plasma adiponectin levels in patients with CKD might play a compensatory role aimed at counteracting renal dysfunction related to MC disorders."},"publication_date":"2009-08","publication_name":{"en":"The Journal of Endocrinology","ja":"The Journal of Endocrinology"},"volume":"Vol.202","number":"No.2","starting_page":"309","ending_page":"316","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1677/JOE-08-0469"],"issn":["1479-6805"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:63, {"insert":{"user_id":"B000337971","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/19262481","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=193054","label":"url"}],"paper_title":{"en":"Adiponectin inhibits insulin-like growth factor-1-induced cell migration by the suppression of extracellular signal-regulated kinase 1/2 activation, but not Akt in vascular smooth muscle cells","ja":"Adiponectin inhibits insulin-like growth factor-1-induced cell migration by the suppression of extracellular signal-regulated kinase 1/2 activation, but not Akt in vascular smooth muscle cells"},"authors":{"en":[{"name":"Motobayashi Yuki"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Ishizawa Keisuke"},{"name":"Orino Sakiko"},{"name":"Yamaguchi Kunihisa"},{"name":"Kawazoe Kazuyoshi"},{"name":"Hamano Shuichi"},{"name":"Tsuchiya Koichiro"},{"name":"Tomita Shuhei"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"Motobayashi Yuki"},{"name":"石澤 有紀"},{"name":"石澤 啓介"},{"name":"Orino Sakiko"},{"name":"山口 邦久"},{"name":"川添 和義"},{"name":"濱野 修一"},{"name":"土屋 浩一郎"},{"name":"冨田 修平"},{"name":"玉置 俊晃"}]},"description":{"en":"Adiponectin, an adipocyte-derived hormone, has been proposed to show antiatherogenic properties through the inhibitory effects against various growth factors. Insulin-like growth factor-1 (IGF-1) is one of the potent mitogens, which has been considered to play important roles in both atherogenesis and plaque stabilization in accordance to the phase of atherosclerosis. The aim of this study is to elucidate the adiponectin effects on IGF-1-induced cell migration and its intracellular signaling pathways in vascular smooth muscle cells (VSMCs). In this study, we assessed cell migration and several kinase activities in cultured rat aortic smooth muscle cells (RASMCs). Adiponectin pretreatment suppressed IGF-1-induced cell migration and extracellular signal-regulated kinase (ERK)1/2 activation, which is one of the major mediators for IGF-1-induced cell migration. In RASMCs, adiponectin and 5-aminoimidazole-4-carboxamide riboside (AICAR), a 5'-AMP-activated protein kinase (AMPK) activator, stimulated AMPK activation. AMPK activation by AICAR inhibited IGF-1-induced ERK1/2 activation and cell migration in RASMCs. On the other hand, phosphorylation of Akt and Bad, proapoptotic molecules of the Bcl-2 family, which were increased by IGF-1 stimulation, was not diminished by the pretreatment with adiponectin. It was shown that adiponectin inhibited IGF-1-induced VSMC migration through suppression of ERK1/2 activation, which might be implicated in AMPK activation. Furthermore, adiponectin selectively inhibited ERK1/2 pathway, not Akt-Bad pathway, stimulated by IGF-1. From these findings, it was implied that adiponectin suppressed IGF-1-induced VSMC migration and its signaling selectivity.","ja":"Adiponectin, an adipocyte-derived hormone, has been proposed to show antiatherogenic properties through the inhibitory effects against various growth factors. Insulin-like growth factor-1 (IGF-1) is one of the potent mitogens, which has been considered to play important roles in both atherogenesis and plaque stabilization in accordance to the phase of atherosclerosis. The aim of this study is to elucidate the adiponectin effects on IGF-1-induced cell migration and its intracellular signaling pathways in vascular smooth muscle cells (VSMCs). In this study, we assessed cell migration and several kinase activities in cultured rat aortic smooth muscle cells (RASMCs). Adiponectin pretreatment suppressed IGF-1-induced cell migration and extracellular signal-regulated kinase (ERK)1/2 activation, which is one of the major mediators for IGF-1-induced cell migration. In RASMCs, adiponectin and 5-aminoimidazole-4-carboxamide riboside (AICAR), a 5'-AMP-activated protein kinase (AMPK) activator, stimulated AMPK activation. AMPK activation by AICAR inhibited IGF-1-induced ERK1/2 activation and cell migration in RASMCs. On the other hand, phosphorylation of Akt and Bad, proapoptotic molecules of the Bcl-2 family, which were increased by IGF-1 stimulation, was not diminished by the pretreatment with adiponectin. It was shown that adiponectin inhibited IGF-1-induced VSMC migration through suppression of ERK1/2 activation, which might be implicated in AMPK activation. Furthermore, adiponectin selectively inhibited ERK1/2 pathway, not Akt-Bad pathway, stimulated by IGF-1. From these findings, it was implied that adiponectin suppressed IGF-1-induced VSMC migration and its signaling selectivity."},"publication_date":"2009-03","publication_name":{"en":"Hypertension Research","ja":"Hypertension Research"},"volume":"Vol.32","number":"No.3","starting_page":"188","ending_page":"193","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1038/hr.2008.19"],"issn":["1348-4214"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:64, {"insert":{"user_id":"B000337971","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/19202317","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=193051","label":"url"}],"paper_title":{"en":"Quercetin Glucuronide Inhibits Cell Migration and Proliferation by Platelet-Derived Growth Factor in Vascular Smooth Muscle Cells","ja":"Quercetin Glucuronide Inhibits Cell Migration and Proliferation by Platelet-Derived Growth Factor in Vascular Smooth Muscle Cells"},"authors":{"en":[{"name":"Ishizawa Keisuke"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Ohnishi Sachiyo"},{"name":"Motobayashi Yuki"},{"name":"Kawazoe Kazuyoshi"},{"name":"Hamano Shuichi"},{"name":"Tsuchiya Koichiro"},{"name":"Tomita Shuhei"},{"name":"Minakuchi Kazuo"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"石澤 啓介"},{"name":"石澤 有紀"},{"name":"Ohnishi Sachiyo"},{"name":"Motobayashi Yuki"},{"name":"川添 和義"},{"name":"濱野 修一"},{"name":"土屋 浩一郎"},{"name":"冨田 修平"},{"name":"水口 和生"},{"name":"玉置 俊晃"}]},"description":{"en":"Many epidemiologic studies have reported that dietary flavonoids provide protection against cardiovascular disease. Quercetin, a member of the bioflavonoids family, has been proposed to have anti-inflammatory, anti-atherogenic, and anti-hypertensive properties leading to the beneficial effects against cardiovascular diseases. Recent studies demonstrated that orally administered quercetin appeared in plasma as glucuronide-conjugated forms in rats and humans. Therefore, we examined the effect of chemically synthesized quercetin glucuronide on platelet-derived growth factor (PDGF)-induced cell migration and kinase activation in cultured rat aortic smooth muscle cells (RASMCs). PDGF-induced RASMC migration was inhibited by quercetin 3-O-beta-D-glucuronide (Q3GA). Q3GA also attenuated PDGF-induced cell proliferation in RASMCs. PDGF activated extracellular-signal regulated kinase (ERK) 1/2, c-Jun N-terminal kinase (JNK), p38 mitogen-activated protein (MAP) kinase, and Akt in RASMCs. PDGF-induced JNK and Akt activations were suppressed by Q3GA, whereas ERK1/2 and p38 MAP kinase activations were not affected. We also confirmed that PDGF-induced JNK and Akt activations were inhibited by antioxidants, N-acetylcysteine and diphenyleneiodonium chloride, in RASMCs. These findings suggest Q3GA would be an active metabolite of quercetin in plasma and may possess preventing effects for cardiovascular diseases relevant to vascular smooth muscle cell disorders.","ja":"Many epidemiologic studies have reported that dietary flavonoids provide protection against cardiovascular disease. Quercetin, a member of the bioflavonoids family, has been proposed to have anti-inflammatory, anti-atherogenic, and anti-hypertensive properties leading to the beneficial effects against cardiovascular diseases. Recent studies demonstrated that orally administered quercetin appeared in plasma as glucuronide-conjugated forms in rats and humans. Therefore, we examined the effect of chemically synthesized quercetin glucuronide on platelet-derived growth factor (PDGF)-induced cell migration and kinase activation in cultured rat aortic smooth muscle cells (RASMCs). PDGF-induced RASMC migration was inhibited by quercetin 3-O-beta-D-glucuronide (Q3GA). Q3GA also attenuated PDGF-induced cell proliferation in RASMCs. PDGF activated extracellular-signal regulated kinase (ERK) 1/2, c-Jun N-terminal kinase (JNK), p38 mitogen-activated protein (MAP) kinase, and Akt in RASMCs. PDGF-induced JNK and Akt activations were suppressed by Q3GA, whereas ERK1/2 and p38 MAP kinase activations were not affected. We also confirmed that PDGF-induced JNK and Akt activations were inhibited by antioxidants, N-acetylcysteine and diphenyleneiodonium chloride, in RASMCs. These findings suggest Q3GA would be an active metabolite of quercetin in plasma and may possess preventing effects for cardiovascular diseases relevant to vascular smooth muscle cell disorders."},"publication_date":"2009-02-07","publication_name":{"en":"Journal of Pharmacological Sciences","ja":"Journal of Pharmacological Sciences"},"volume":"Vol.109","number":"No.2","starting_page":"257","ending_page":"264","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1254/jphs.08236FP"],"issn":["1347-8613"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:65, {"insert":{"user_id":"B000337971","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/18753302","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=189061","label":"url"}],"paper_title":{"en":"Dietary doses of nitrite restore circulating nitric oxide level and improve renal injury in L-NAME-induced hypertensive rats","ja":"Dietary doses of nitrite restore circulating nitric oxide level and improve renal injury in L-NAME-induced hypertensive rats"},"authors":{"en":[{"name":"Kanematsu Yasuhisa"},{"name":"Yamaguchi Kunihisa"},{"name":"Ohnishi Hideki"},{"name":"Motobayashi Yuki"},{"name":"Ishizawa Keisuke"},{"name":"Izawa Yuki"},{"name":"Kawazoe Kazuyoshi"},{"name":"Kondo Shuji"},{"name":"Kagami Shoji"},{"name":"Tomita Shuhei"},{"name":"Tsuchiya Koichiro"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"兼松 康久"},{"name":"山口 邦久"},{"name":"大西 秀樹"},{"name":"元林 有紀"},{"name":"石澤 啓介"},{"name":"井澤 有紀"},{"name":"川添 和義"},{"name":"近藤 秀治"},{"name":"香美 祥二"},{"name":"冨田 修平"},{"name":"土屋 浩一郎"},{"name":"玉置 俊晃"}]},"description":{"en":"We have reported that pharmacological doses of oral nitrite increase circulating nitric oxide (NO) and exert hypotensive effects in Nomega-nitro-L-arginine methyl ester (L-NAME)-induced hypertensive rats. In this study, we examined the effect of a chronic dietary dose of nitrite on the hypertension and renal damage induced by chronic L-NAME administration in rats. The animals were administered tap water containing L-NAME (1 g/l) or L-NAME + nitrite (low dose: 0.1 mg/l, medium dose: 1 mg/l, high dose: 10 mg/l) for 8 wk. We evaluated blood NO levels as hemoglobin-NO adducts (iron-nitrosyl-hemoglobin), using an electron paramagnetic resonance method. Chronic administration of L-NAME for 8 wk induced hypertension and renal injury and reduced the blood iron-nitrosyl-hemoglobin level (control 38.8 +/- 8.9 vs. L-NAME 6.0 +/- 3.1 arbitrary units). Coadministration of a low dose of nitrite with L-NAME did not change the reduced iron-nitrosyl-hemoglobin signal and did not improve the L-NAME-induced renal injury. The blood iron-nitrosyl-hemoglobin signals of the medium dose and high dose of nitrite were significantly higher than that of L-NAME alone. Chronic administration of a medium dose of nitrite attenuated L-NAME-induced renal histological changes and proteinuria. A high dose of nitrite also attenuated L-NAME-induced renal injury. These findings suggest that dietary doses of nitrite that protect the kidney are associated with significant increase in iron-nitrosyl-hemoglobin levels. We conclude that dietary nitrite-derived NO generation may serve as a backup system when the nitric oxide synthase/L-arginine-dependent NO generation system is compromised.","ja":"We have reported that pharmacological doses of oral nitrite increase circulating nitric oxide (NO) and exert hypotensive effects in Nomega-nitro-L-arginine methyl ester (L-NAME)-induced hypertensive rats. In this study, we examined the effect of a chronic dietary dose of nitrite on the hypertension and renal damage induced by chronic L-NAME administration in rats. The animals were administered tap water containing L-NAME (1 g/l) or L-NAME + nitrite (low dose: 0.1 mg/l, medium dose: 1 mg/l, high dose: 10 mg/l) for 8 wk. We evaluated blood NO levels as hemoglobin-NO adducts (iron-nitrosyl-hemoglobin), using an electron paramagnetic resonance method. Chronic administration of L-NAME for 8 wk induced hypertension and renal injury and reduced the blood iron-nitrosyl-hemoglobin level (control 38.8 +/- 8.9 vs. L-NAME 6.0 +/- 3.1 arbitrary units). Coadministration of a low dose of nitrite with L-NAME did not change the reduced iron-nitrosyl-hemoglobin signal and did not improve the L-NAME-induced renal injury. The blood iron-nitrosyl-hemoglobin signals of the medium dose and high dose of nitrite were significantly higher than that of L-NAME alone. Chronic administration of a medium dose of nitrite attenuated L-NAME-induced renal histological changes and proteinuria. A high dose of nitrite also attenuated L-NAME-induced renal injury. These findings suggest that dietary doses of nitrite that protect the kidney are associated with significant increase in iron-nitrosyl-hemoglobin levels. We conclude that dietary nitrite-derived NO generation may serve as a backup system when the nitric oxide synthase/L-arginine-dependent NO generation system is compromised."},"publication_date":"2008-08-27","publication_name":{"en":"American Journal of Physiology, Renal Physiology","ja":"American Journal of Physiology, Renal Physiology"},"volume":"Vol.295","number":"No.5","starting_page":"F1457","ending_page":"F1462","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1152/ajprenal.00621.2007"],"issn":["1931-857X"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:66, {"insert":{"user_id":"B000337971","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/18250560","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=176515","label":"url"}],"paper_title":{"en":"Big mitogen-activated protein kinase 1 (BMK1)/extracellular signal regulated kinase 5 (ERK5) is involved in platelet-derived growth factor (PDGF)-induced vascular smooth muscle cell migration","ja":"Big mitogen-activated protein kinase 1 (BMK1)/extracellular signal regulated kinase 5 (ERK5) is involved in platelet-derived growth factor (PDGF)-induced vascular smooth muscle cell migration"},"authors":{"en":[{"name":"Izawa Yuki"},{"name":"Yoshizumi Masanori"},{"name":"Ishizawa Keisuke"},{"name":"Fujita Yoshiko"},{"name":"Kondo Shuji"},{"name":"Kagami Shoji"},{"name":"Kawazoe Kazuyoshi"},{"name":"Tsuchiya Koichiro"},{"name":"Tomita Shuhei"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"井澤 有紀"},{"name":"吉栖 正典"},{"name":"石澤 啓介"},{"name":"Fujita Yoshiko"},{"name":"近藤 秀治"},{"name":"香美 祥二"},{"name":"川添 和義"},{"name":"土屋 浩一郎"},{"name":"冨田 修平"},{"name":"玉置 俊晃"}]},"description":{"en":"Big mitogen-activated protein kinase 1 (BMK1), also known as extracellular signal-regulated kinase 5 (ERK5), is a newly identified member of the mitogen-activated protein (MAP) kinase family. Recently, several studies have suggested that BMK1 plays an important role in the pathogenesis of cardiovascular disease. To clarify the pathophysiological significance of BMK1 in the process of vascular remodeling, we explored the molecular mechanisms of BMK1 activation in vascular smooth muscle cells (VSMCs). From the results of co-immunoprecipitation and immunoblotting analyses, it was found that platelet-derived growth factor (PDGF), a known potent mitogen, activated BMK1 and triggered the Gab1-SHP-2 interaction in rat aortic smooth muscle cells (RASMCs). The abrogation of SHP-2 phosphatase activity by transfection of the SHP-2-C/S mutant suppressed PDGF-stimulated BMK1 activation. Infection with an adenoviral vector expressing dominant-negative MEK5alpha, which can suppress PDGF-stimulated BMK1 activation to the control level, inhibited PDGF-induced RASMC migration. Moreover, we observed an increase of BMK1 activation in injured mouse femoral arteries. From these findings, it is suggested that BMK1 activation leads to VSMC migration induced by PDGF via Gab1-SHP-2 interaction, and that BMK1-mediated VSMC migration may play a role in the pathogenesis of vascular remodeling.","ja":"Big mitogen-activated protein kinase 1 (BMK1), also known as extracellular signal-regulated kinase 5 (ERK5), is a newly identified member of the mitogen-activated protein (MAP) kinase family. Recently, several studies have suggested that BMK1 plays an important role in the pathogenesis of cardiovascular disease. To clarify the pathophysiological significance of BMK1 in the process of vascular remodeling, we explored the molecular mechanisms of BMK1 activation in vascular smooth muscle cells (VSMCs). From the results of co-immunoprecipitation and immunoblotting analyses, it was found that platelet-derived growth factor (PDGF), a known potent mitogen, activated BMK1 and triggered the Gab1-SHP-2 interaction in rat aortic smooth muscle cells (RASMCs). The abrogation of SHP-2 phosphatase activity by transfection of the SHP-2-C/S mutant suppressed PDGF-stimulated BMK1 activation. Infection with an adenoviral vector expressing dominant-negative MEK5alpha, which can suppress PDGF-stimulated BMK1 activation to the control level, inhibited PDGF-induced RASMC migration. Moreover, we observed an increase of BMK1 activation in injured mouse femoral arteries. From these findings, it is suggested that BMK1 activation leads to VSMC migration induced by PDGF via Gab1-SHP-2 interaction, and that BMK1-mediated VSMC migration may play a role in the pathogenesis of vascular remodeling."},"publication_date":"2007-11","publication_name":{"en":"Hypertension Research","ja":"Hypertension Research"},"volume":"Vol.30","number":"No.11","starting_page":"1107","ending_page":"1117","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1291/hypres.30.1107"],"issn":["0916-9636"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:67, {"insert":{"user_id":"B000337971","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/16832158","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=160310","label":"url"}],"paper_title":{"en":"Effects of angiotensin II type 1 receptor blockade on the systemic blood nitric oxide dynamics in Nω-nitro-L-arginine methyl ester-treated rats","ja":"Effects of angiotensin II type 1 receptor blockade on the systemic blood nitric oxide dynamics in Nω-nitro-L-arginine methyl ester-treated rats"},"authors":{"en":[{"name":"Kanematsu Yasuhisa"},{"name":"Tsuchiya Koichiro"},{"name":"Onishi Hideki"},{"name":"Motobayashi Yuki"},{"name":"Izawa Yuki"},{"name":"Ishihara Manabu"},{"name":"Ishizawa Keisuke"},{"name":"Abe Shinji"},{"name":"Kawazoe Kazuyoshi"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"兼松 康久"},{"name":"土屋 浩一郎"},{"name":"大西 秀樹"},{"name":"元林 有紀"},{"name":"井澤 有紀"},{"name":"石原 学"},{"name":"石澤 啓介"},{"name":"阿部 真治"},{"name":"川添 和義"},{"name":"玉置 俊晃"}]},"description":{"en":"We previously succeeded in measuring the nitrosylhemoglobin (HbNO) level as an index of blood nitric oxide (NO) by the electron paramagnetic resonance (EPR) HbNO signal subtraction method. In this study, we examined the effects of olmesartan, an angiotensin II type 1 receptor blocker (ARB), on NO dynamics in N(omega)-nitro-L-arginine methyl ester (L-NAME)-treated rats by the EPR-subtraction method. Oral administration of L-NAME for 2 weeks induced serious hypertension, and the HbNO concentration was reduced to 37.6% of the level in controls. Coadministration of olmesartan improved hypertension and increased the blood HbNO concentration of L-NAME-treated rats. In contrast, coadministration of hydralazine improved hypertension but did not affect the blood HbNO concentration. In conclusion, our findings suggested that chronic administration of olmesartan ameliorated the endothelial dysfunction in L-NAME-treated rats.","ja":"We previously succeeded in measuring the nitrosylhemoglobin (HbNO) level as an index of blood nitric oxide (NO) by the electron paramagnetic resonance (EPR) HbNO signal subtraction method. In this study, we examined the effects of olmesartan, an angiotensin II type 1 receptor blocker (ARB), on NO dynamics in N(omega)-nitro-L-arginine methyl ester (L-NAME)-treated rats by the EPR-subtraction method. Oral administration of L-NAME for 2 weeks induced serious hypertension, and the HbNO concentration was reduced to 37.6% of the level in controls. Coadministration of olmesartan improved hypertension and increased the blood HbNO concentration of L-NAME-treated rats. In contrast, coadministration of hydralazine improved hypertension but did not affect the blood HbNO concentration. In conclusion, our findings suggested that chronic administration of olmesartan ameliorated the endothelial dysfunction in L-NAME-treated rats."},"publication_date":"2006-05","publication_name":{"en":"Hypertension Research","ja":"Hypertension Research"},"volume":"Vol.29","number":"No.5","starting_page":"369","ending_page":"374","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1291/hypres.29.369"],"issn":["0916-9636"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:68, {"insert":{"user_id":"B000337971","type":"published_papers","id":"32296483"},"force":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/16322069","label":"url"},{"@id":"https://www.scopus.com/record/display.url?eid=2-s2.0-32644452665&origin=inward","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=139866","label":"url"}],"paper_title":{"en":"Transactivation of fetal liver kinase-1/kinase-insert domain-containing receptor by lysophosphatidylcholine induces vascular endothelial cell proliferation.","ja":"Transactivation of fetal liver kinase-1/kinase-insert domain-containing receptor by lysophosphatidylcholine induces vascular endothelial cell proliferation."},"authors":{"en":[{"name":"Fujita Yoshiko"},{"name":"Yoshizumi Masanori"},{"name":"Izawa Yuki"},{"name":"Ali Nermin"},{"name":"Kanematsu Yasuhisa"},{"name":"Ishizawa Keisuke"},{"name":"Tsuchiya Koichiro"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"藤田 佳子"},{"name":"吉栖 正典"},{"name":"井澤 有紀"},{"name":"アリ ネルミン"},{"name":"兼松 康久"},{"name":"石澤 啓介"},{"name":"土屋 浩一郎"},{"name":"玉置 俊晃"}]},"description":{"en":"Lysophosphatidylcholine (LPC), a major lipid component of oxidized low-density lipoprotein, is a bioactive lipid molecule involved in numerous biological processes including the progression of atherosclerosis. Recently orphan G protein-coupled receptors were identified as high-affinity receptors for LPC. Although several G protein-coupled receptor ligands transactivate receptor tyrosine kinases, LPC-stimulated transactivation of receptor tyrosine kinase has not yet been reported. Here we observed for the first time that LPC treatment of human umbilical vein endothelial cells (HUVECs) induces tyrosyl phosphorylation of vascular endothelial growth factor receptor 2 [fetal liver kinase-1/kinase-insert domain-containing receptor, Flk-1/KDR)]. Flk-1/KDR transactivation by LPC was inhibited by vascular endothelial growth factor receptor tyrosine kinase inhibitors, SU1498 and 4-[(4'-chloro-2'-fluoro) phenylamino]6,7-dimethoxyquinazoline (VTKi) in immunoprecipitation. Furthermore, we examined the effects of the Src family kinases inhibitors, herbimycin A and 4-amino-5-(4-chlorophenyl)-7-(t-butyl) pyrazolo[3,4-d] pyrimidine (PP2), on LPC-induced Flk-1/KDR transactivation. Results from Western blots, c-Src is involved in LPC-induced Flk-1/KDR transactivation because herbimycin A and PP2 inhibited this transactivation. Kinase-inactive (KI) Src transfection also inhibited LPC-induced Flk-1/KDR transactivation. In addition, results from Western blots, ERK1/2 and Akt, which are downstream effectors of Flk-1/KDR, were also activated by LPC, and this was inhibited by SU1498, VTKi, herbimycin A, PP2, and KI Src transfection in HUVECs. LPC-induced stimulation of HUVEC proliferation was shown to be secondary to transactivation because it was suppressed by SU1498, VTKi, herbimycin A, PP2, and KI Src transfection in dimethylthiazoldiphenyltetra-zoliumbromide assay. These findings suggest that LPC-induced Flk-1/KDR transactivation via c-Src may have important implications for the progression of atherosclerosis.","ja":"Lysophosphatidylcholine (LPC), a major lipid component of oxidized low-density lipoprotein, is a bioactive lipid molecule involved in numerous biological processes including the progression of atherosclerosis. Recently orphan G protein-coupled receptors were identified as high-affinity receptors for LPC. Although several G protein-coupled receptor ligands transactivate receptor tyrosine kinases, LPC-stimulated transactivation of receptor tyrosine kinase has not yet been reported. Here we observed for the first time that LPC treatment of human umbilical vein endothelial cells (HUVECs) induces tyrosyl phosphorylation of vascular endothelial growth factor receptor 2 [fetal liver kinase-1/kinase-insert domain-containing receptor, Flk-1/KDR)]. Flk-1/KDR transactivation by LPC was inhibited by vascular endothelial growth factor receptor tyrosine kinase inhibitors, SU1498 and 4-[(4'-chloro-2'-fluoro) phenylamino]6,7-dimethoxyquinazoline (VTKi) in immunoprecipitation. Furthermore, we examined the effects of the Src family kinases inhibitors, herbimycin A and 4-amino-5-(4-chlorophenyl)-7-(t-butyl) pyrazolo[3,4-d] pyrimidine (PP2), on LPC-induced Flk-1/KDR transactivation. Results from Western blots, c-Src is involved in LPC-induced Flk-1/KDR transactivation because herbimycin A and PP2 inhibited this transactivation. Kinase-inactive (KI) Src transfection also inhibited LPC-induced Flk-1/KDR transactivation. In addition, results from Western blots, ERK1/2 and Akt, which are downstream effectors of Flk-1/KDR, were also activated by LPC, and this was inhibited by SU1498, VTKi, herbimycin A, PP2, and KI Src transfection in HUVECs. LPC-induced stimulation of HUVEC proliferation was shown to be secondary to transactivation because it was suppressed by SU1498, VTKi, herbimycin A, PP2, and KI Src transfection in dimethylthiazoldiphenyltetra-zoliumbromide assay. These findings suggest that LPC-induced Flk-1/KDR transactivation via c-Src may have important implications for the progression of atherosclerosis."},"publication_date":"2006-03","publication_name":{"en":"Endocrinology","ja":"Endocrinology"},"volume":"Vol.147","number":"No.3","starting_page":"1377","ending_page":"1385","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1210/en.2005-0644"],"issn":["0013-7227"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:69, {"insert":{"user_id":"B000337971","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/16362428","label":"url"},{"@id":"https://www.scopus.com/record/display.url?eid=2-s2.0-31144433876&origin=inward","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=161673","label":"url"}],"paper_title":{"en":"Pramipexole protects against H2O2-induced PC12 cell death","ja":"Pramipexole protects against H2O2-induced PC12 cell death"},"authors":{"en":[{"name":"Fujita Yoshiko"},{"name":"Izawa Yuki"},{"name":"Ali Nermin"},{"name":"Tsuchiya Koichiro"},{"name":"Hamano Shuichi"},{"name":"Tamaki Toshiaki"},{"name":"Yoshizumi Masanori"}],"ja":[{"name":"藤田 佳子"},{"name":"井澤 有紀"},{"name":"アリ ネルミン"},{"name":"土屋 浩一郎"},{"name":"濱野 修一"},{"name":"玉置 俊晃"},{"name":"吉栖 正典"}]},"description":{"en":"Pramipexole, a novel non-ergot dopamine (DA) agonist, has been successfully applied to the treatment of Parkinson's disease (PD). Although the specific cause of PD remains unknown, recent studies have provided evidence that oxidative stress plays a role in the parthenogenesis of the disease. In the present study, we examined the effect of pramipexole on hydrogen peroxide (H2O2, 100 microM)-induced PC12 cell death, and the intracellular mechanism of this effect. The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium (MTT) assay revealed that pretreatment of PC12 cells with pramipexole (1-100 microM) resulted in significant protection against H2O2-induced cell death in a concentration-dependent manner. The protective effect of pramipexole was not affected by pretreatment with the DA receptor antagonists sulpiride, spiperone or domperidone, suggesting that the effect of pramipexole is not mediated by DA receptors. In PC12 cells, pramipexole inhibited H2O2-induced lactate dehydrogenase (LDH) leakage, as well as H2O2-induced cytochrome c release and caspase-3 activation with the resultant apoptosis. It was also observed in PC12 cells that H2O2 stimulated phosphorylation of mitogen-activated protein (MAP) kinases, i.e., extracellular signal-regulated kinase1/2 (ERK1/2), c-Jun NH2-terminal kinase (JNK) and p38 MAP kinase. Pramipexole inhibited H2O2-induced JNK and p38 MAP kinase, but not ERK1/2 phosphorylation. Furthermore, in these cells experiments with a fluorescent probe, 2-[6-(4'-amino)phenoxy-3H-xanthen-3-on-9-yl]benzoic acid, revealed that pramipexole, the JNK inhibitor SP600125 and the p38 MAP kinase inhibitor SB203580 inhibited the generation of H2O2-induced reactive oxygen species. Caspase inhibitors Z-DEVD-FMK and Z-IETD-FMK, as well as SP600125 and SB203580, inhibited H2O2-induced PC12 cell death to a similar extent as pramipexole. These results suggest that pramipexole exerts a protective effect against oxidative stress-induced PC12 cell death in part through an inhibition of JNK and p38 MAP kinase.","ja":"Pramipexole, a novel non-ergot dopamine (DA) agonist, has been successfully applied to the treatment of Parkinson's disease (PD). Although the specific cause of PD remains unknown, recent studies have provided evidence that oxidative stress plays a role in the parthenogenesis of the disease. In the present study, we examined the effect of pramipexole on hydrogen peroxide (H2O2, 100 microM)-induced PC12 cell death, and the intracellular mechanism of this effect. The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium (MTT) assay revealed that pretreatment of PC12 cells with pramipexole (1-100 microM) resulted in significant protection against H2O2-induced cell death in a concentration-dependent manner. The protective effect of pramipexole was not affected by pretreatment with the DA receptor antagonists sulpiride, spiperone or domperidone, suggesting that the effect of pramipexole is not mediated by DA receptors. In PC12 cells, pramipexole inhibited H2O2-induced lactate dehydrogenase (LDH) leakage, as well as H2O2-induced cytochrome c release and caspase-3 activation with the resultant apoptosis. It was also observed in PC12 cells that H2O2 stimulated phosphorylation of mitogen-activated protein (MAP) kinases, i.e., extracellular signal-regulated kinase1/2 (ERK1/2), c-Jun NH2-terminal kinase (JNK) and p38 MAP kinase. Pramipexole inhibited H2O2-induced JNK and p38 MAP kinase, but not ERK1/2 phosphorylation. Furthermore, in these cells experiments with a fluorescent probe, 2-[6-(4'-amino)phenoxy-3H-xanthen-3-on-9-yl]benzoic acid, revealed that pramipexole, the JNK inhibitor SP600125 and the p38 MAP kinase inhibitor SB203580 inhibited the generation of H2O2-induced reactive oxygen species. Caspase inhibitors Z-DEVD-FMK and Z-IETD-FMK, as well as SP600125 and SB203580, inhibited H2O2-induced PC12 cell death to a similar extent as pramipexole. These results suggest that pramipexole exerts a protective effect against oxidative stress-induced PC12 cell death in part through an inhibition of JNK and p38 MAP kinase."},"publication_date":"2006-01","publication_name":{"en":"Naunyn-Schmiedeberg's Archives of Pharmacology","ja":"Naunyn-Schmiedeberg's Archives of Pharmacology"},"volume":"Vol.372","number":"No.4","starting_page":"257","ending_page":"266","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1007/s00210-005-0025-2"],"issn":["0028-1298"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:70, {"insert":{"user_id":"B000337971","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/111587","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/16366521","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=133901","label":"url"}],"paper_title":{"en":"Effects of forced swimming stress on rat brain function","ja":"Effects of forced swimming stress on rat brain function"},"authors":{"en":[{"name":"Sakakibara Hiroyuki"},{"name":"Ishida Kaori"},{"name":"Izawa Yuki"},{"name":"Minami Yuko"},{"name":"Saito Satomi"},{"name":"Kawai Yoshichika"},{"name":"Butterweck Veronika"},{"name":"Tamaki Toshiaki"},{"name":"Nakaya Yutaka"},{"name":"Terao Junji"}],"ja":[{"name":"Sakakibara Hiroyuki"},{"name":"Ishida Kaori"},{"name":"井澤 有紀"},{"name":"Minami Yuko"},{"name":"Saito Satomi"},{"name":"河合 慶親"},{"name":"Butterweck Veronika"},{"name":"玉置 俊晃"},{"name":"中屋 豊"},{"name":"寺尾 純二"}]},"description":{"en":"Chronic stress has been reported to be an essential factor for depression. In this study, the effect of forced swimming stress on neurotransmitters and cellular signaling pathway contributing to brain functions was investigated using the forced swimming test (FST) in order to understanding of mechanisms to regulate stress signals in brain. Antidepressant drug, imipramine, significantly reduced the immobility time of male rats in the FST by 85% at a dose of 15 mg/kg for 2 weeks. This result indicated that the swimming stress caused a depressed state in the rats without administration of imipramine. Swimming stress significantly lowered the serotonergic ratio and also markedly enhanced the phosphorylation of ERK1/2 in the hypothalamus region compared to the rats without FST. These phenomena may be included in key mechanisms of the development of depression.","ja":"Chronic stress has been reported to be an essential factor for depression. In this study, the effect of forced swimming stress on neurotransmitters and cellular signaling pathway contributing to brain functions was investigated using the forced swimming test (FST) in order to understanding of mechanisms to regulate stress signals in brain. Antidepressant drug, imipramine, significantly reduced the immobility time of male rats in the FST by 85% at a dose of 15 mg/kg for 2 weeks. This result indicated that the swimming stress caused a depressed state in the rats without administration of imipramine. Swimming stress significantly lowered the serotonergic ratio and also markedly enhanced the phosphorylation of ERK1/2 in the hypothalamus region compared to the rats without FST. These phenomena may be included in key mechanisms of the development of depression."},"publication_date":"2005-12-01","publication_name":{"en":"The Journal of Medical Investigation : JMI","ja":"The Journal of Medical Investigation : JMI"},"volume":"Vol.52","number":"No.Suppl.","starting_page":"300","ending_page":"3001","languages":["eng"],"referee":true,"identifiers":{"doi":["10.2152/jmi.52.300"],"issn":["1343-1420"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:71, {"insert":{"user_id":"B000337971","type":"published_papers","id":"32296484"},"force":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/15921682","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=131104","label":"url"}],"paper_title":{"en":"ERK1/2 activation by angiotensin II inhibits insulin-induced glucose uptake in vascular smooth muscle cells","ja":"ERK1/2 activation by angiotensin II inhibits insulin-induced glucose uptake in vascular smooth muscle cells"},"authors":{"en":[{"name":"Izawa Yuki"},{"name":"Yoshizumi Masanori"},{"name":"Ishizawa Keisuke"},{"name":"Fujita Yoshiko"},{"name":"Kondo Shuji"},{"name":"Kagami Shoji"},{"name":"Kawazoe Kazuyoshi"},{"name":"Tsuchiya Koichiro"},{"name":"Tomita Shuhei"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"井澤 有紀"},{"name":"吉栖 正典"},{"name":"石澤 啓介"},{"name":"藤田 佳子"},{"name":"近藤 秀治"},{"name":"香美 祥二"},{"name":"川添 和義"},{"name":"土屋 浩一郎"},{"name":"冨田 修平"},{"name":"玉置 俊晃"}]},"description":{"en":"Clinical evidence suggests a relationship between hypertension and insulin resistance, and cross-talk between angiotensin II (Ang II) and insulin signaling pathways may take place. We now report the effect of Ang II on insulin-induced glucose uptake and its intracellular mechanisms in vascular smooth muscle cells (VSMC). We examined the translocation of glucose transporter-4 (GLUT-4) and glucose uptake in rat aortic smooth muscle cells (RASMC). Mitogen-activated protein (MAP) kinases and Akt activities, and phosphorylation of insulin receptor substrate-1 (IRS-1) at the serine and tyrosine residues were measured by immunoprecipitation and immunoblotting. As a result, Ang II inhibited insulin-induced GLUT-4 translocation from cytoplasm to the plasma membrane in RASMC. Ang II induced extracellular signal-regulated kinase (ERK) 1/2 and c-Jun N-terminal kinase (JNK) activation and IRS-1 phosphorylation at Ser307 and Ser616. Ang II-induced Ser307 and Ser616 phophorylation of IRS-1 was inhibited by a MEK inhibitor, PD98059, and a JNK inhibitor, SP600125. Ang II inhibition of insulin-stimulated IRS-1 tyrosyl phophorylation and Akt activation were reversed by PD98059 but not by SP600125. Ang II inhibited insulin-induced glucose uptake, which was also reversed by PD98059 but not by SP600125. It is shown that Ang II-induced ERK1/2 activation inhibits insulin-dependent glucose uptake through serine phophorylation of IRS-1 in RASMC.","ja":"Clinical evidence suggests a relationship between hypertension and insulin resistance, and cross-talk between angiotensin II (Ang II) and insulin signaling pathways may take place. We now report the effect of Ang II on insulin-induced glucose uptake and its intracellular mechanisms in vascular smooth muscle cells (VSMC). We examined the translocation of glucose transporter-4 (GLUT-4) and glucose uptake in rat aortic smooth muscle cells (RASMC). Mitogen-activated protein (MAP) kinases and Akt activities, and phosphorylation of insulin receptor substrate-1 (IRS-1) at the serine and tyrosine residues were measured by immunoprecipitation and immunoblotting. As a result, Ang II inhibited insulin-induced GLUT-4 translocation from cytoplasm to the plasma membrane in RASMC. Ang II induced extracellular signal-regulated kinase (ERK) 1/2 and c-Jun N-terminal kinase (JNK) activation and IRS-1 phosphorylation at Ser307 and Ser616. Ang II-induced Ser307 and Ser616 phophorylation of IRS-1 was inhibited by a MEK inhibitor, PD98059, and a JNK inhibitor, SP600125. Ang II inhibition of insulin-stimulated IRS-1 tyrosyl phophorylation and Akt activation were reversed by PD98059 but not by SP600125. Ang II inhibited insulin-induced glucose uptake, which was also reversed by PD98059 but not by SP600125. It is shown that Ang II-induced ERK1/2 activation inhibits insulin-dependent glucose uptake through serine phophorylation of IRS-1 in RASMC."},"publication_date":"2005-08-15","publication_name":{"en":"Experimental Cell Research","ja":"Experimental Cell Research"},"volume":"Vol.308","number":"No.2","starting_page":"291","ending_page":"299","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1016/j.yexcr.2005.04.028"],"issn":["0014-4827"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:72, {"insert":{"user_id":"B000337971","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/16087789","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=139855","label":"url"}],"paper_title":{"en":"Aldosterone stimulates vascular smooth muscle cell proliferation via big mitoten-activated protein kinase 1 activation","ja":"Aldosterone stimulates vascular smooth muscle cell proliferation via big mitoten-activated protein kinase 1 activation"},"authors":{"en":[{"name":"Ishizawa Keisuke"},{"name":"Izawa Yuki"},{"name":"Ito Hiroyuki"},{"name":"Miki Chieko"},{"name":"Miyama Kayoko"},{"name":"Fujita Yoshiko"},{"name":"Kanematsu Yasuhisa"},{"name":"Tsuchiya Koichiro"},{"name":"Tamaki Toshiaki"},{"name":"Nishiyama Akira"},{"name":"Yoshizumi Masanori"}],"ja":[{"name":"石澤 啓介"},{"name":"井澤 有紀"},{"name":"伊藤 浩敬"},{"name":"Miki Chieko"},{"name":"Miyama Kayoko"},{"name":"藤田 佳子"},{"name":"兼松 康久"},{"name":"土屋 浩一郎"},{"name":"玉置 俊晃"},{"name":"西山 成"},{"name":"吉栖 正典"}]},"description":{"en":"The nongenomic effects of aldosterone have been implicated in the pathogenesis of various cardiovascular diseases. Aldosterone-induced nongenomic effects are attributable in part to the activation of extracellular signal-regulated kinase 1/2 (ERK1/2), a classical mitogen-activated protein (MAP) kinase. Big MAP kinase 1 (BMK1), a newly identified MAP kinase, has been shown to be involved in cell proliferation, differentiation, and survival. We examined whether aldosterone stimulates BMK1-mediated proliferation of cultured rat aortic smooth muscle cells (RASMCs). Mineralocorticoid receptor (MR) expression and localization were evaluated by Western blotting analysis and fluorolabeling methods. ERK1/2 and BMK1 activities were measured by Western blotting analysis with the respective phosphospecific antibodies. Cell proliferation was determined by Alamar Blue colorimetric assay. Aldosterone (0.1 to 100 nmol/L) dose-dependently activated BMK1 in RASMCs, with a peak at 30 minutes. To clarify whether aldosterone-induced BMK1 activation is an MR-mediated phenomenon, we examined the effect of eplerenone, a selective MR antagonist, on aldosterone-induced BMK1 activation. Eplerenone (0.1 to 10 micromol/L) dose-dependently inhibited aldosterone-induced BMK1 activation in RASMCs. Aldosterone also stimulated RASMC proliferation, which was inhibited by eplerenone. Aldosterone-mediated phenomena were concluded to be attributable to a nongenomic effect because cycloheximide failed to inhibit aldosterone-induced BMK1 activation. Transfection of dominant-negative MAP kinase/ERK kinase 5 (MEK5), which is an upstream regulator of BMK1, partially inhibited aldosterone-induced RASMC proliferation, which was almost completely inhibited by MEK inhibitor PD98059. In addition to the classical steroid activity, rapid nongenomic effects induced by aldosterone may represent an alternative etiology for vascular diseases such as hypertension.","ja":"The nongenomic effects of aldosterone have been implicated in the pathogenesis of various cardiovascular diseases. Aldosterone-induced nongenomic effects are attributable in part to the activation of extracellular signal-regulated kinase 1/2 (ERK1/2), a classical mitogen-activated protein (MAP) kinase. Big MAP kinase 1 (BMK1), a newly identified MAP kinase, has been shown to be involved in cell proliferation, differentiation, and survival. We examined whether aldosterone stimulates BMK1-mediated proliferation of cultured rat aortic smooth muscle cells (RASMCs). Mineralocorticoid receptor (MR) expression and localization were evaluated by Western blotting analysis and fluorolabeling methods. ERK1/2 and BMK1 activities were measured by Western blotting analysis with the respective phosphospecific antibodies. Cell proliferation was determined by Alamar Blue colorimetric assay. Aldosterone (0.1 to 100 nmol/L) dose-dependently activated BMK1 in RASMCs, with a peak at 30 minutes. To clarify whether aldosterone-induced BMK1 activation is an MR-mediated phenomenon, we examined the effect of eplerenone, a selective MR antagonist, on aldosterone-induced BMK1 activation. Eplerenone (0.1 to 10 micromol/L) dose-dependently inhibited aldosterone-induced BMK1 activation in RASMCs. Aldosterone also stimulated RASMC proliferation, which was inhibited by eplerenone. Aldosterone-mediated phenomena were concluded to be attributable to a nongenomic effect because cycloheximide failed to inhibit aldosterone-induced BMK1 activation. Transfection of dominant-negative MAP kinase/ERK kinase 5 (MEK5), which is an upstream regulator of BMK1, partially inhibited aldosterone-induced RASMC proliferation, which was almost completely inhibited by MEK inhibitor PD98059. In addition to the classical steroid activity, rapid nongenomic effects induced by aldosterone may represent an alternative etiology for vascular diseases such as hypertension."},"publication_date":"2005-08-08","publication_name":{"en":"Hypertension","ja":"Hypertension"},"volume":"Vol.46","number":"No.4","starting_page":"1046","ending_page":"1052","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1161/01.HYP.0000172622.51973.f5"],"issn":["1524-4563"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:73, {"insert":{"user_id":"B000337971","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/15961403","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=241203","label":"url"}],"paper_title":{"en":"Androgen receptor gene knockout male mice exhibit impaired cardiac growth and exacerbation of angiotensin II-induced cardiac fibrosis.","ja":"Androgen receptor gene knockout male mice exhibit impaired cardiac growth and exacerbation of angiotensin II-induced cardiac fibrosis."},"authors":{"en":[{"name":"Ikeda Yasumasa"},{"name":"Aihara Ken-ichi"},{"name":"Sato Takashi"},{"name":"Akaike Masashi"},{"name":"Yoshizumi Masanori"},{"name":"Suzaki Yuki"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Fujimura Mitsunori"},{"name":"Hashizume Shunji"},{"name":"Kato Midori"},{"name":"Yagi Shusuke"},{"name":"Tamaki Toshiaki"},{"name":"Kawano Hirotaka"},{"name":"Matsumoto Takahiro"},{"name":"Azuma Hiroyuki"},{"name":"Kato Shigeaki"},{"name":"Matsumoto Toshio"}],"ja":[{"name":"池田 康将"},{"name":"粟飯原 賢一"},{"name":"Sato Takashi"},{"name":"赤池 雅史"},{"name":"吉栖 正典"},{"name":"Suzaki Yuki"},{"name":"石澤 有紀"},{"name":"Fujimura Mitsunori"},{"name":"Hashizume Shunji"},{"name":"Kato Midori"},{"name":"八木 秀介"},{"name":"玉置 俊晃"},{"name":"Kawano Hirotaka"},{"name":"松本 高広"},{"name":"東 博之"},{"name":"Kato Shigeaki"},{"name":"松本 俊夫"}]},"description":{"en":"Androgen has anabolic effects on cardiac myocytes and has been shown to enhance left ventricular enlargement and function. However, the physiological and patho-physiological roles of androgen in cardiac growth and cardiac stress-induced remodeling remains unclear. We aimed to clarify whether the androgen-nuclear androgen receptor (AR) system contributes to the cardiac growth and angiotensin II (Ang II)-stimulated cardiac remodeling by using systemic AR-null male mice. AR knock-out (ARKO) male mice, at 25 weeks of age, and age-matched wild-type (WT) male mice were treated with or without Ang II stimulation (2.0 mg/kg/day) for 2 weeks. ARKO mice with or without Ang II stimulation showed a significant reduction in the heart-to-body weight ratio compared with those of WT mice. In addition, echocardiographic analysis demonstrated impairments of both the concentric hypertrophic response and left ventricular function in Ang II-stimulated ARKO mice. Western blot analysis of the myocardium revealed that activation of extracellular signal-regulated kinases (ERK) 1/2 and ERK5 by Ang II stimulation were lower in ARKO mice than those of WT mice. Ang II stimulation caused more prominent cardiac fibrosis in ARKO mice than in WT mice with enhanced expression of types I and III collagen and transforming growth factor-beta1 genes and with increased Smad2 activation. These results suggest that, in male mice, the androgen-AR system participates in normal cardiac growth and modulates cardiac adaptive hypertrophy and fibrosis during the process of cardiac remodeling under hypertrophic stress.","ja":"Androgen has anabolic effects on cardiac myocytes and has been shown to enhance left ventricular enlargement and function. However, the physiological and patho-physiological roles of androgen in cardiac growth and cardiac stress-induced remodeling remains unclear. We aimed to clarify whether the androgen-nuclear androgen receptor (AR) system contributes to the cardiac growth and angiotensin II (Ang II)-stimulated cardiac remodeling by using systemic AR-null male mice. AR knock-out (ARKO) male mice, at 25 weeks of age, and age-matched wild-type (WT) male mice were treated with or without Ang II stimulation (2.0 mg/kg/day) for 2 weeks. ARKO mice with or without Ang II stimulation showed a significant reduction in the heart-to-body weight ratio compared with those of WT mice. In addition, echocardiographic analysis demonstrated impairments of both the concentric hypertrophic response and left ventricular function in Ang II-stimulated ARKO mice. Western blot analysis of the myocardium revealed that activation of extracellular signal-regulated kinases (ERK) 1/2 and ERK5 by Ang II stimulation were lower in ARKO mice than those of WT mice. Ang II stimulation caused more prominent cardiac fibrosis in ARKO mice than in WT mice with enhanced expression of types I and III collagen and transforming growth factor-beta1 genes and with increased Smad2 activation. These results suggest that, in male mice, the androgen-AR system participates in normal cardiac growth and modulates cardiac adaptive hypertrophy and fibrosis during the process of cardiac remodeling under hypertrophic stress."},"publication_date":"2005-06-16","publication_name":{"en":"The Journal of Biological Chemistry","ja":"The Journal of Biological Chemistry"},"volume":"Vol.280","number":"No.33","starting_page":"29661","ending_page":"29666","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1074/jbc.M411694200"],"issn":["0021-9258"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:74, {"insert":{"user_id":"B000337971","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"http://www.jstage.jst.go.jp/article/jphs/98/2/98_130/_article/-char/ja/","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/15937404","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=131109","label":"url"}],"paper_title":{"en":"A Novel Src Kinase Inhibitor, M475271, Inhibits VEGF-Induced Human Umbilical Vein Endothelial Cell Proliferation and Migration","ja":"A Novel Src Kinase Inhibitor, M475271, Inhibits VEGF-Induced Human Umbilical Vein Endothelial Cell Proliferation and Migration"},"authors":{"en":[{"name":"Nermin Ali"},{"name":"Yoshizumi Masanori"},{"name":"Fujita Yoshiko"},{"name":"Izawa Yuki"},{"name":"Kanematsu Yasuhisa"},{"name":"Ishizawa Keisuke"},{"name":"Tsuchiya Koichiro"},{"name":"Yano Seiji"},{"name":"Sone Saburo"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"Nermin Ali"},{"name":"吉栖 正典"},{"name":"Fujita Yoshiko"},{"name":"井澤 有紀"},{"name":"兼松 康久"},{"name":"石澤 啓介"},{"name":"土屋 浩一郎"},{"name":"矢野 聖二"},{"name":"曽根 三郎"},{"name":"玉置 俊晃"}]},"description":{"en":"Vascular endothelial growth factor (VEGF) was reported to be a potent proangiogenic factor that plays a pivotal role in both physiological and pathological angiogenesis. M475271, 4-quinazolinamine, N-(2-chloro-5-methoxyphenyl)-6-methoxy-7-[(1-methyl-4-piperidinyl) methoxy]-(9Cl), is a new anilinoquinazoline derivative that showed selective inhibition of Src kinase activity and tumor growth in vivo. Here, we examined the effect of M475271 on VEGF-induced human umbilical vein endothelial cell (HUVEC) proliferation and migration and their intracellular mechanisms. Our findings showed that M475271 pretreatment resulted in a significant inhibition of VEGF-induced HUVEC proliferation, [(3)H]thymidine incorporation, and migration. M475271 inhibited VEGF-induced Flk-1 and Src phosphorylation and their association. Confocal laser microscopic examination confirmed the inhibitory effect of M475271 on VEGF-induced Flk-1/Src association. M475271 inhibited VEGF-induced extracellular signal-regulated kinase1/2 (ERK1/2) and p38 but not Akt activation in a concentration-dependent manner. M475271, PI3-K inhibitor, and p38 inhibitor inhibited VEGF-induced HUVEC proliferation and migration. However, a MEK1/2 inhibitor inhibited VEGF-induced proliferation but not migration. These findings suggest that M475271 attenuates VEGF-induced HUVEC proliferation and migration through the inhibition of signaling pathways involving Src, ERK1/2, and/or p38. Taken together, these data indicate that M475271 may be a useful candidate for inhibition of endothelial cell proliferation and migration relevant to angiogenesis.","ja":"Vascular endothelial growth factor (VEGF) was reported to be a potent proangiogenic factor that plays a pivotal role in both physiological and pathological angiogenesis. M475271, 4-quinazolinamine, N-(2-chloro-5-methoxyphenyl)-6-methoxy-7-[(1-methyl-4-piperidinyl) methoxy]-(9Cl), is a new anilinoquinazoline derivative that showed selective inhibition of Src kinase activity and tumor growth in vivo. Here, we examined the effect of M475271 on VEGF-induced human umbilical vein endothelial cell (HUVEC) proliferation and migration and their intracellular mechanisms. Our findings showed that M475271 pretreatment resulted in a significant inhibition of VEGF-induced HUVEC proliferation, [(3)H]thymidine incorporation, and migration. M475271 inhibited VEGF-induced Flk-1 and Src phosphorylation and their association. Confocal laser microscopic examination confirmed the inhibitory effect of M475271 on VEGF-induced Flk-1/Src association. M475271 inhibited VEGF-induced extracellular signal-regulated kinase1/2 (ERK1/2) and p38 but not Akt activation in a concentration-dependent manner. M475271, PI3-K inhibitor, and p38 inhibitor inhibited VEGF-induced HUVEC proliferation and migration. However, a MEK1/2 inhibitor inhibited VEGF-induced proliferation but not migration. These findings suggest that M475271 attenuates VEGF-induced HUVEC proliferation and migration through the inhibition of signaling pathways involving Src, ERK1/2, and/or p38. Taken together, these data indicate that M475271 may be a useful candidate for inhibition of endothelial cell proliferation and migration relevant to angiogenesis."},"publication_date":"2005-06-04","publication_name":{"en":"Journal of Pharmacological Sciences","ja":"Journal of Pharmacological Sciences"},"volume":"Vol.98","number":"No.2","starting_page":"130","ending_page":"141","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1254/jphs.FP0040850"],"issn":["1347-8613"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:75, {"insert":{"user_id":"B000337971","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"http://ajpheart.physiology.org/cgi/content/abstract/288/5/H2163","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/15626692","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=131097","label":"url"}],"paper_title":{"en":"Nitrite is an alternative source of NO in vivo","ja":"Nitrite is an alternative source of NO in vivo"},"authors":{"en":[{"name":"Tsuchiya Koichiro"},{"name":"Kanematsu Yasuhisa"},{"name":"Yoshizumi Masanori"},{"name":"Ohnishi Hideki"},{"name":"Kirima Kazuyoshi"},{"name":"Izawa Yuki"},{"name":"Shikishima Michiyo"},{"name":"Ishida Tatsuhiro"},{"name":"Kondo Shuji"},{"name":"Kagami Shoji"},{"name":"Takiguchi Yoshiharu"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"土屋 浩一郎"},{"name":"兼松 康久"},{"name":"Yoshizumi Masanori"},{"name":"Ohnishi Hideki"},{"name":"Kirima Kazuyoshi"},{"name":"井澤 有紀"},{"name":"Shikishima Michiyo"},{"name":"石田 竜弘"},{"name":"Kondo Shuji"},{"name":"香美 祥二"},{"name":"滝口 祥令"},{"name":"玉置 俊晃"}]},"description":{"en":"In this study, we investigated whether orally administered nitrite is changed to NO and whether nitrite attenuates hypertension in a dose-dependent manner. We utilized a stable isotope of [15N]nitrite (15NO2-) as a source of nitrite to distinguish between endogenous nitrite and that exogenously administered and measured hemoglobin (Hb)-NO as an index of circulating NO in whole blood using electron paramagnetic resonance (EPR) spectroscopy. When 1 mg/kg Na15NO2 was orally administered to rats, an apparent EPR signal derived from Hb15NO (A(Z) = 23.4 gauss) appeared in the blood. The peak blood HbNO concentration occurred at the first measurement after intake (5 min) for treatment with 1 and 3 mg/kg (HbNO: 4.93 +/- 0.52 and 10.58 +/- 0.40 microM, respectively) and at 15 min with 10 mg/kg (HbNO: 38.27 +/- 9.23 microM). In addition, coadministration of nitrite (100 mg/l drinking water) with N(omega)-nitro-L-arginine methyl ester (L-NAME; 1 g/l) for 3 wk significantly attenuated the L-NAME-induced hypertension (149 +/- 10 mmHg) compared with L-NAME alone (170 +/- 13 mmHg). Furthermore, this phenomenon was associated with an increase in circulating HbNO. Our findings clearly indicate that orally ingested nitrite can be an alternative to L-arginine as a source of NO in vivo and may explain, at least in part, the mechanism of the nitrite/nitrate-rich Dietary Approaches to Stop Hypertension diet-induced hypotensive effects.","ja":"In this study, we investigated whether orally administered nitrite is changed to NO and whether nitrite attenuates hypertension in a dose-dependent manner. We utilized a stable isotope of [15N]nitrite (15NO2-) as a source of nitrite to distinguish between endogenous nitrite and that exogenously administered and measured hemoglobin (Hb)-NO as an index of circulating NO in whole blood using electron paramagnetic resonance (EPR) spectroscopy. When 1 mg/kg Na15NO2 was orally administered to rats, an apparent EPR signal derived from Hb15NO (A(Z) = 23.4 gauss) appeared in the blood. The peak blood HbNO concentration occurred at the first measurement after intake (5 min) for treatment with 1 and 3 mg/kg (HbNO: 4.93 +/- 0.52 and 10.58 +/- 0.40 microM, respectively) and at 15 min with 10 mg/kg (HbNO: 38.27 +/- 9.23 microM). In addition, coadministration of nitrite (100 mg/l drinking water) with N(omega)-nitro-L-arginine methyl ester (L-NAME; 1 g/l) for 3 wk significantly attenuated the L-NAME-induced hypertension (149 +/- 10 mmHg) compared with L-NAME alone (170 +/- 13 mmHg). Furthermore, this phenomenon was associated with an increase in circulating HbNO. Our findings clearly indicate that orally ingested nitrite can be an alternative to L-arginine as a source of NO in vivo and may explain, at least in part, the mechanism of the nitrite/nitrate-rich Dietary Approaches to Stop Hypertension diet-induced hypotensive effects."},"publication_date":"2005-05","publication_name":{"en":"American Journal of Physiology, Heart and Circulatory Physiology","ja":"American Journal of Physiology, Heart and Circulatory Physiology"},"volume":"Vol.288","number":"No.5","starting_page":"H2163","ending_page":"H2170","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1152/ajpheart.00525.2004"],"issn":["0363-6135"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:76, {"insert":{"user_id":"B000337971","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/15367387","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=113756","label":"url"}],"paper_title":{"en":"Nitrite-derived nitric oxide formation following ischemia-reperfusion injyury in kidney.","ja":"Nitrite-derived nitric oxide formation following ischemia-reperfusion injyury in kidney."},"authors":{"en":[{"name":"Okamoto Masumi"},{"name":"Tsuchiya Koichiro"},{"name":"Kanematsu Yasuhisa"},{"name":"Izawa Yuki"},{"name":"Yoshizumi Masanori"},{"name":"Kagawa Susumu"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"岡本 増巳"},{"name":"土屋 浩一郎"},{"name":"兼松 康久"},{"name":"井澤 有紀"},{"name":"吉栖 正典"},{"name":"香川 征"},{"name":"玉置 俊晃"}]},"description":{"en":"Nitric oxide (NO) is synthesized from l-arginine by nitric oxide synthase (NOS), and nitrite and nitrate are believed to be waste forms of NO. We previously reported an enzyme-independent pathway of NO generation from nitrite in acidic conditions. In this study, we show nitrite-derived NO formation in renal ischemia-reperfusion injury using electron paramagnetic resonance (EPR) spectroscopy. In this experiment, we utilized a stable isotope of [(15)N]nitrite as a source of nitrite to distinguish l-arginine-derived NO from [(15)N]nitrite-derived (15)NO. Intravenous infusion of a stable isotope of [(15)N]nitrite ((15)NO(2)(-)) facilitated the formation of Hb(15)NO during renal ischemia, which demonstrated that the origin of NO was nitrite. The EPR signal of Hb(15)NO in kidney appeared after 40 min of renal ischemia, and renal reperfusion decreased the Hb(15)NO level in the kidney and increased it in blood by contrast. In addition, the amount of HbNO was nitrite concentration dependent, and this formation was NOS independent. Our findings suggest that nitrite can be an alternative source of NO in ischemic kidney and that it binds with hemoglobin and then is spread by the circulation after reperfusion.","ja":"Nitric oxide (NO) is synthesized from l-arginine by nitric oxide synthase (NOS), and nitrite and nitrate are believed to be waste forms of NO. We previously reported an enzyme-independent pathway of NO generation from nitrite in acidic conditions. In this study, we show nitrite-derived NO formation in renal ischemia-reperfusion injury using electron paramagnetic resonance (EPR) spectroscopy. In this experiment, we utilized a stable isotope of [(15)N]nitrite as a source of nitrite to distinguish l-arginine-derived NO from [(15)N]nitrite-derived (15)NO. Intravenous infusion of a stable isotope of [(15)N]nitrite ((15)NO(2)(-)) facilitated the formation of Hb(15)NO during renal ischemia, which demonstrated that the origin of NO was nitrite. The EPR signal of Hb(15)NO in kidney appeared after 40 min of renal ischemia, and renal reperfusion decreased the Hb(15)NO level in the kidney and increased it in blood by contrast. In addition, the amount of HbNO was nitrite concentration dependent, and this formation was NOS independent. Our findings suggest that nitrite can be an alternative source of NO in ischemic kidney and that it binds with hemoglobin and then is spread by the circulation after reperfusion."},"publication_date":"2005","publication_name":{"en":"American Journal of Physiology, Renal Physiology","ja":"American Journal of Physiology, Renal Physiology"},"volume":"Vol.288","number":"No.1","starting_page":"182","ending_page":"187","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1152/ajprenal.00036.2004"],"issn":["1931-857X"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:77, {"insert":{"user_id":"B000337971","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"http://www.jstage.jst.go.jp/article/jphs/96/4/96_395/_article/-char/ja/","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/15599101","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=131093","label":"url"}],"paper_title":{"en":"Malfunction of vascular control in lifestyle-related diseases : formation of systemic hemoglobin-nitric oxide Complex(HbNO) From Dietary Nitrite","ja":"Malfunction of vascular control in lifestyle-related diseases : formation of systemic hemoglobin-nitric oxide Complex(HbNO) From Dietary Nitrite"},"authors":{"en":[{"name":"Tsuchiya Koichiro"},{"name":"Takiguchi Yoshiharu"},{"name":"Okamoto Masumi"},{"name":"Izawa Yuki"},{"name":"Kanematsu Yasuhisa"},{"name":"Yoshizumi Masanori"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"土屋 浩一郎"},{"name":"滝口 祥令"},{"name":"Okamoto Masumi"},{"name":"井澤 有紀"},{"name":"兼松 康久"},{"name":"Yoshizumi Masanori"},{"name":"玉置 俊晃"}]},"description":{"en":"Nitric oxide (NO) has many physiological functions. It is believed to be produced from L-arginine by nitric oxide synthase (NOS), and nitrite and nitrate are waste forms of it. By the way, nitrate and nitrite are abundant in vegetables and fruits, especially leafy vegetables and pickled vegetables. Orally-ingested nitrate is changed to nitrite by micro-organelles living in the hypopharynx area, and nitrite is expected to change to NO in the stomach due to its low pH. Indeed, some researchers reported that NO is produced in the gastric cavity, although few reports mentioned the physiological meanings of this NO formation. Therefore, we investigated whether the nitrite-derived NO can shift to the circulation and acts like NOS-derived NO does in tissues. We adopted a stable isotope of nitrite (15NO2-) in order to distinguish between the endogenous nitrite and the exogenously administered one and measured nitrosyl hemoglobin (HbNO) as an index of circulating NO using electron paramagnetic resonance spectroscopy. It appeared that the oral administration of 15N-nitrite formed the Hb15NO in rat blood and decreased the blood pressure of chronic L-NAME treated rats. Our findings suggest that the intake of nitrite (or nitrate)-rich foods such as vegetables and fruits would alter the systemic HbNO dynamism, resulting in the improvement of cardiovascular diseases.","ja":"Nitric oxide (NO) has many physiological functions. It is believed to be produced from L-arginine by nitric oxide synthase (NOS), and nitrite and nitrate are waste forms of it. By the way, nitrate and nitrite are abundant in vegetables and fruits, especially leafy vegetables and pickled vegetables. Orally-ingested nitrate is changed to nitrite by micro-organelles living in the hypopharynx area, and nitrite is expected to change to NO in the stomach due to its low pH. Indeed, some researchers reported that NO is produced in the gastric cavity, although few reports mentioned the physiological meanings of this NO formation. Therefore, we investigated whether the nitrite-derived NO can shift to the circulation and acts like NOS-derived NO does in tissues. We adopted a stable isotope of nitrite (15NO2-) in order to distinguish between the endogenous nitrite and the exogenously administered one and measured nitrosyl hemoglobin (HbNO) as an index of circulating NO using electron paramagnetic resonance spectroscopy. It appeared that the oral administration of 15N-nitrite formed the Hb15NO in rat blood and decreased the blood pressure of chronic L-NAME treated rats. Our findings suggest that the intake of nitrite (or nitrate)-rich foods such as vegetables and fruits would alter the systemic HbNO dynamism, resulting in the improvement of cardiovascular diseases."},"publication_date":"2004-12-10","publication_name":{"en":"Journal of Pharmacological Sciences","ja":"Journal of Pharmacological Sciences"},"volume":"Vol.96","number":"No.4","starting_page":"395","ending_page":"400","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1254/jphs.FMJ04006X3"],"issn":["1347-8613"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:78, {"insert":{"user_id":"B000337971","type":"published_papers","id":"32296485"},"force":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/15297771","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=113755","label":"url"}],"paper_title":{"en":"Antioxidant effects of stereoisomers of N-acetylcysteine (NAC), L-NAC and D-NAC, on angiotensin II-stimulated MAP kinase activation and vascular smooth muscle cell proliferation","ja":"Antioxidant effects of stereoisomers of N-acetylcysteine (NAC), L-NAC and D-NAC, on angiotensin II-stimulated MAP kinase activation and vascular smooth muscle cell proliferation"},"authors":{"en":[{"name":"Kyaw Moe"},{"name":"Yoshizumi Masanori"},{"name":"Tsuchiya Koichiro"},{"name":"Izawa Yuki"},{"name":"Kanematsu Yasuhisa"},{"name":"Fujita Yoshiko"},{"name":"Ali Nermin"},{"name":"Ishizawa Keisuke"},{"name":"Yamauchi Aiko"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"Kyaw Moe"},{"name":"吉栖 正典"},{"name":"土屋 浩一郎"},{"name":"井澤 有紀"},{"name":"兼松 康久"},{"name":"藤田 佳子"},{"name":"Ali Nermin"},{"name":"石澤 啓介"},{"name":"山内 あい子"},{"name":"玉置 俊晃"}]},"description":{"en":"We examined the effects of the stereoisomers of N-acetylcysteine (NAC), L-NAC and D-NAC, on cellular glutathione (GSH) concentration and whether NAC-regulated cellular GSH levels are directly associated with angiotensin II (Ang II)-induced intracellular signaling events in vascular smooth muscle cells (VSMC). Both L-NAC and D-NAC similarly increased intracellular GSH concentration. We found that L-NAC and D-NAC both inhibited Ang II-induced c-Jun N-terminal kinase and p38 mitogen-activated protein kinase activation and [(3)H]-thymidine incorporation in VSMC. Our present study indicates the comparable effects of NAC stereoisomers in regulating intracellular GSH and the redox-dependent intracellular signaling mechanisms in VSMC.","ja":"We examined the effects of the stereoisomers of N-acetylcysteine (NAC), L-NAC and D-NAC, on cellular glutathione (GSH) concentration and whether NAC-regulated cellular GSH levels are directly associated with angiotensin II (Ang II)-induced intracellular signaling events in vascular smooth muscle cells (VSMC). Both L-NAC and D-NAC similarly increased intracellular GSH concentration. We found that L-NAC and D-NAC both inhibited Ang II-induced c-Jun N-terminal kinase and p38 mitogen-activated protein kinase activation and [(3)H]-thymidine incorporation in VSMC. Our present study indicates the comparable effects of NAC stereoisomers in regulating intracellular GSH and the redox-dependent intracellular signaling mechanisms in VSMC."},"publication_date":"2004-08-05","publication_name":{"en":"Journal of Pharmacological Sciences","ja":"Journal of Pharmacological Sciences"},"volume":"Vol.95","number":"No.4","starting_page":"483","ending_page":"486","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1254/jphs.SC0040061"],"issn":["1347-8613"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:79, {"insert":{"user_id":"B000337971","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"http://www.chinaphar.com/1671-4083/25/977.htm","label":"url"},{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/15301727","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=131089","label":"url"}],"paper_title":{"en":"Atheroprotective effects of antioxidants through inhibition of mitogen-activated protein kinases","ja":"Atheroprotective effects of antioxidants through inhibition of mitogen-activated protein kinases"},"authors":{"en":[{"name":"Kyaw Moe"},{"name":"Yoshizumi Masanori"},{"name":"Tsuchiya Koichiro"},{"name":"Izawa Yuki"},{"name":"Kanematsu Yasuhisa"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"Kyaw Moe"},{"name":"Yoshizumi Masanori"},{"name":"土屋 浩一郎"},{"name":"井澤 有紀"},{"name":"兼松 康久"},{"name":"玉置 俊晃"}]},"description":{"en":"Reactive oxygen species (ROS) have been known to play an important role in the pathogenesis of atherosclerosis and several other cardiovascular diseases. It is now apparent that ROS induce endothelial cell damage and vascular smooth muscle cell (VSMC) growth and cardiac remodeling, which are associated with hypertension, atherosclerosis, heart failure, and restenosis. Several lines of evidence have indicated that ROS and mitogen-activated protein (MAP) kinases were involved in vascular remodeling under various pathological conditions. Recently, it was also reported that MAP kinases were sensitive to oxidative stress. MAP kinases play an important role in cell differentiation, growth, apoptosis, and the regulation of a variety of transcription factors and gene expressions. Bioflavonoids and polyphenolic compounds are believed to be beneficial for the prevention and treatment of atherosclerosis and cardiovascular diseases. One of the most widely distributed bioflavonoids, 3,3',4',5,7-penta-hydroxyflavone (quercetin) and its metabolite quercetin 3-O-beta-D-glucuronide (Q3GA) inhibited Angiotensin II-stimulated JNK activation and resultant hypertrophy of VSMC. Several studies have suggested that various antioxidants including probucol, N-acetyl-L-cysteine, diphenylene iodonium, Trolox C (vitamin E analogue), and vitamin C inhibit VSMC growth, which is associated with pathogenesis of cardiovascular diseases. Therefore, inhibition of MAP kinases by antioxidant treatment may prove to be a therapeutic strategy for cardiovascular diseases. In contrast, some clinical studies have reported that antioxidant vitamins did not show beneficial effects in coronary artery disease or in a number of high-risk people. Thus, further studies are needed to clarify why antioxidants showed beneficial effects in vitro, whereas less satisfactory results were obtained in some clinical conditions.","ja":"Reactive oxygen species (ROS) have been known to play an important role in the pathogenesis of atherosclerosis and several other cardiovascular diseases. It is now apparent that ROS induce endothelial cell damage and vascular smooth muscle cell (VSMC) growth and cardiac remodeling, which are associated with hypertension, atherosclerosis, heart failure, and restenosis. Several lines of evidence have indicated that ROS and mitogen-activated protein (MAP) kinases were involved in vascular remodeling under various pathological conditions. Recently, it was also reported that MAP kinases were sensitive to oxidative stress. MAP kinases play an important role in cell differentiation, growth, apoptosis, and the regulation of a variety of transcription factors and gene expressions. Bioflavonoids and polyphenolic compounds are believed to be beneficial for the prevention and treatment of atherosclerosis and cardiovascular diseases. One of the most widely distributed bioflavonoids, 3,3',4',5,7-penta-hydroxyflavone (quercetin) and its metabolite quercetin 3-O-beta-D-glucuronide (Q3GA) inhibited Angiotensin II-stimulated JNK activation and resultant hypertrophy of VSMC. Several studies have suggested that various antioxidants including probucol, N-acetyl-L-cysteine, diphenylene iodonium, Trolox C (vitamin E analogue), and vitamin C inhibit VSMC growth, which is associated with pathogenesis of cardiovascular diseases. Therefore, inhibition of MAP kinases by antioxidant treatment may prove to be a therapeutic strategy for cardiovascular diseases. In contrast, some clinical studies have reported that antioxidant vitamins did not show beneficial effects in coronary artery disease or in a number of high-risk people. Thus, further studies are needed to clarify why antioxidants showed beneficial effects in vitro, whereas less satisfactory results were obtained in some clinical conditions."},"publication_date":"2004-08","publication_name":{"en":"Acta Pharmacologica Sinica","ja":"Acta Pharmacologica Sinica"},"volume":"Vol.25","number":"No.8","starting_page":"977","ending_page":"985","languages":["eng"],"referee":true,"identifiers":{"issn":["1671-4083"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:80, {"insert":{"user_id":"B000337971","type":"published_papers","id":"32296486"},"force":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/15253109","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=113754","label":"url"}],"paper_title":{"en":"Dual effects of endothelin-1 (1-31): induction of mesangial cell migration and facilitation of monocyte recruitment through monocyte chemoattractant protein-1 production by mesangial cells","ja":"Dual effects of endothelin-1 (1-31): induction of mesangial cell migration and facilitation of monocyte recruitment through monocyte chemoattractant protein-1 production by mesangial cells"},"authors":{"en":[{"name":"Ishizawa Keisuke"},{"name":"Yoshizumi Masanori"},{"name":"Tsuchiya Koichiro"},{"name":"Houchi Hitoshi"},{"name":"Minakuchi Kazuo"},{"name":"Izawa Yuki"},{"name":"Kanematsu Yasuhisa"},{"name":"Kagami Shoji"},{"name":"Hirose Masao"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"石澤 啓介"},{"name":"吉栖 正典"},{"name":"土屋 浩一郎"},{"name":"芳地 一"},{"name":"水口 和生"},{"name":"井澤 有紀"},{"name":"兼松 康久"},{"name":"香美 祥二"},{"name":"Hirose Masao"},{"name":"玉置 俊晃"}]},"description":{"en":"We previously found that human chymase selectively cleaves big endothelin-1 (ET-1) at the Tyr31-Gly32 bond and produces 31-amino acid endothelins, ET-1 (1-31), without any further degradation products. In this study, we investigated the effect of ET-1 (1-31) on the migration of cultured rat mesangial cells (RMCs) and on cells of the human monocytic cell line, THP-1. In addition, we examined the interaction between RMCs and THP-1 cells using conditioned media from ET-1 (1-31)-stimulated RMCs. ET-1 (1-31) caused an increase in RMC migration in a concentration-dependent manner, and the degree of increase was similar to those by ET-1 and angiotensin II (All). The ET-1 (1-31)-induced increase in RMC migration was inhibited by BQ123, an endothelin ETA receptor antagonist, but not by BQ788, an endothelin ETB receptor antagonist. ET-1 (1-31) alone did not cause significant migration of THP-1 cells. However, significant recruitment of THP-1 cells was observed with conditioned media taken from ET-1 (1-31)-stimulated RMCs. The conditioned media-induced migration of THP-1 cells was inhibited by BQ123, but not by BQ788. Western blotting analysis of the lysate of RMCs revealed that the expression of monocyte chemoattractant protein-1 (MCP-1) protein in RMCs was increased by treatment with ET-1 (1-31). The addition of neutralizing antibody for MCP-1 to the medium inhibited the migration of THP-1 cells induced by conditioned media from ET-1 (1-31)-stimulated RMCs. These findings suggest that ET-1 (1-31) play a role in glomerulonephritis (GN) via dual effects that directly cause the migration of mesangial cells (MCs) and may be responsible for the recruitment of mononuclear cells mediated through the activation of MCs. Since human chymase has been reported to be involved in glomerular disease, ET-1 (1-31) may be among the mediators.","ja":"We previously found that human chymase selectively cleaves big endothelin-1 (ET-1) at the Tyr31-Gly32 bond and produces 31-amino acid endothelins, ET-1 (1-31), without any further degradation products. In this study, we investigated the effect of ET-1 (1-31) on the migration of cultured rat mesangial cells (RMCs) and on cells of the human monocytic cell line, THP-1. In addition, we examined the interaction between RMCs and THP-1 cells using conditioned media from ET-1 (1-31)-stimulated RMCs. ET-1 (1-31) caused an increase in RMC migration in a concentration-dependent manner, and the degree of increase was similar to those by ET-1 and angiotensin II (All). The ET-1 (1-31)-induced increase in RMC migration was inhibited by BQ123, an endothelin ETA receptor antagonist, but not by BQ788, an endothelin ETB receptor antagonist. ET-1 (1-31) alone did not cause significant migration of THP-1 cells. However, significant recruitment of THP-1 cells was observed with conditioned media taken from ET-1 (1-31)-stimulated RMCs. The conditioned media-induced migration of THP-1 cells was inhibited by BQ123, but not by BQ788. Western blotting analysis of the lysate of RMCs revealed that the expression of monocyte chemoattractant protein-1 (MCP-1) protein in RMCs was increased by treatment with ET-1 (1-31). The addition of neutralizing antibody for MCP-1 to the medium inhibited the migration of THP-1 cells induced by conditioned media from ET-1 (1-31)-stimulated RMCs. These findings suggest that ET-1 (1-31) play a role in glomerulonephritis (GN) via dual effects that directly cause the migration of mesangial cells (MCs) and may be responsible for the recruitment of mononuclear cells mediated through the activation of MCs. Since human chymase has been reported to be involved in glomerular disease, ET-1 (1-31) may be among the mediators."},"publication_date":"2004-06","publication_name":{"en":"Hypertension Research","ja":"Hypertension Research"},"volume":"Vol.27","number":"No.6","starting_page":"433","ending_page":"440","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1291/hypres.27.433"],"issn":["0916-9636"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:81, {"insert":{"user_id":"B000337971","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/15086914","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=90670","label":"url"}],"paper_title":{"en":"BMK1 is activated in glomeruli of diabetic rats and in mesangial cells by high glucose conditions","ja":"BMK1 is activated in glomeruli of diabetic rats and in mesangial cells by high glucose conditions"},"authors":{"en":[{"name":"Suzaki Yuki"},{"name":"Yoshizumi Masanori"},{"name":"Kagami Shoji"},{"name":"Nishiyama Akira"},{"name":"Ozawa Yuichi"},{"name":"Kyaw Moe"},{"name":"Izawa Yuki"},{"name":"Kanematsu Yasuhisa"},{"name":"Tsuchiya Koichiro"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"須崎 友紀"},{"name":"吉栖 正典"},{"name":"香美 祥二"},{"name":"西山 成"},{"name":"小澤 祐一"},{"name":"モーチョー"},{"name":"井澤 有紀"},{"name":"兼松 康久"},{"name":"土屋 浩一郎"},{"name":"玉置 俊晃"}]},"description":{"en":"High glucose causes renal cell injury through various signal transduction pathways, including mitogen-activated protein (MAP) kinases cascades. Big MAP kinase 1 (BMK1), also known as extracellular signal-regulated kinase 5 (ERK5), is a recently identified MAP kinase family member and was reported to be sensitive to osmotic and oxidative stress. However, the role of BMK1 in diabetic nephropathy has not been elucidated yet. We investigated whether BMK1 is activated in the glomeruli of Otsuka Long Evans Tokushima Fatty (OLETF) rats, a model of type 2 diabetes mellitus in comparison with the control Long Evans Tokushima Otsuka (LETO) rats. We also examined the effect of high glucose on BMK1 activity in cultured rat mesangial cells. BMK1 and ERK1/2 but not p38 were activated in the glomeruli of OLETF rats, which showed diabetic nephropathy at 52 weeks of age. High glucose, in addition to a high concentration of raffinose, caused rapid and significant activation of BMK1 in rat mesangial cells. MAP kinase/ERK kinase (MEK) inhibitors, U0126 and PD98059, both inhibited BMK1 activation by high glucose in a concentration-dependent manner. Protein kinase C (PKC) inhibition by GF109203X and PKC down-regulation with long-time phorbol myristate acetate (PMA) treatment both inhibited BMK1 and Src kinase activation. Src kinase inhibitors, herbimycin A and PP2, also inhibited high glucose-induced BMK1 activation. PKC inhibitors, Src inhibitors and MEK inhibitors, all inhibited cell proliferation by high glucose. Finally, transfection of dominant-negative MEK5, which is an upstream regulator of BMK1, abolished the BMK1-mediated rat mesangial cell proliferation stimulated by high glucose. In the present study, we demonstrated that high glucose activates BMK1 both in vivo and in vitro. It was suggested that high glucose induces PKC- and c-Src-dependent BMK1 activation. It could not be denied that BMK1 activation is induced through an osmotic stress-sensitive mechanism. BMK1-mediated mesangial cell growth may be involved in the pathogenesis of diabetic nephropathy.","ja":"High glucose causes renal cell injury through various signal transduction pathways, including mitogen-activated protein (MAP) kinases cascades. Big MAP kinase 1 (BMK1), also known as extracellular signal-regulated kinase 5 (ERK5), is a recently identified MAP kinase family member and was reported to be sensitive to osmotic and oxidative stress. However, the role of BMK1 in diabetic nephropathy has not been elucidated yet. We investigated whether BMK1 is activated in the glomeruli of Otsuka Long Evans Tokushima Fatty (OLETF) rats, a model of type 2 diabetes mellitus in comparison with the control Long Evans Tokushima Otsuka (LETO) rats. We also examined the effect of high glucose on BMK1 activity in cultured rat mesangial cells. BMK1 and ERK1/2 but not p38 were activated in the glomeruli of OLETF rats, which showed diabetic nephropathy at 52 weeks of age. High glucose, in addition to a high concentration of raffinose, caused rapid and significant activation of BMK1 in rat mesangial cells. MAP kinase/ERK kinase (MEK) inhibitors, U0126 and PD98059, both inhibited BMK1 activation by high glucose in a concentration-dependent manner. Protein kinase C (PKC) inhibition by GF109203X and PKC down-regulation with long-time phorbol myristate acetate (PMA) treatment both inhibited BMK1 and Src kinase activation. Src kinase inhibitors, herbimycin A and PP2, also inhibited high glucose-induced BMK1 activation. PKC inhibitors, Src inhibitors and MEK inhibitors, all inhibited cell proliferation by high glucose. Finally, transfection of dominant-negative MEK5, which is an upstream regulator of BMK1, abolished the BMK1-mediated rat mesangial cell proliferation stimulated by high glucose. In the present study, we demonstrated that high glucose activates BMK1 both in vivo and in vitro. It was suggested that high glucose induces PKC- and c-Src-dependent BMK1 activation. It could not be denied that BMK1 activation is induced through an osmotic stress-sensitive mechanism. BMK1-mediated mesangial cell growth may be involved in the pathogenesis of diabetic nephropathy."},"publication_date":"2004-04","publication_name":{"en":"Kidney International","ja":"Kidney International"},"volume":"Vol.65","number":"No.5","starting_page":"1749","ending_page":"1760","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1111/j.1523-1755.2004.00576.x"],"issn":["0085-2538"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:82, {"insert":{"user_id":"B000337971","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/15044612","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=90579","label":"url"}],"paper_title":{"en":"Src and Cas are essentially but differentially involved in angiotensin II-stimulated migration of vascular smooth muscle cell via extracellur signal-regulated kinase 1/2 and c-Jun NH2-terminal kinase activation","ja":"Src and Cas are essentially but differentially involved in angiotensin II-stimulated migration of vascular smooth muscle cell via extracellur signal-regulated kinase 1/2 and c-Jun NH2-terminal kinase activation"},"authors":{"en":[{"name":"Kyaw Moe"},{"name":"Yoshizumi Masanori"},{"name":"Tsuchiya Koichiro"},{"name":"Kagami Shoji"},{"name":"Izawa Yuki"},{"name":"Fujita Yoshiko"},{"name":"Ali Nermin"},{"name":"Kanematsu Yasuhisa"},{"name":"Toida Kazunori"},{"name":"Ishimura Kazunori"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"モーチョー"},{"name":"吉栖 正典"},{"name":"土屋 浩一郎"},{"name":"香美 祥二"},{"name":"井澤 有紀"},{"name":"藤田 佳子"},{"name":"ネルミン アリ"},{"name":"兼松 康久"},{"name":"樋田 一徳"},{"name":"石村 和敬"},{"name":"玉置 俊晃"}]},"description":{"en":"Angiotensin II (Ang II) plays an important role in several cardiovascular diseases associated with vascular smooth muscle cell (VSMC) growth and migration. Src activity is known to be required for the migration of a number of cell types. p130Cas was reported to be essential for cell migration and actin filament reorganization. Mitogen-activated protein (MAP) kinases were also reported to be critical regulatory factors for growth and migration of VSMC. However, precise intracellular mechanisms involving c-Src, p130Cas, and MAP kinases in Ang II-stimulated migration of VSMC have not been well elucidated. Here we demonstrated that Ang II rapidly and significantly stimulated tyrosine phosphorylation of Src and Cas and their association in rat aortic smooth muscle cells (RASMC). Ang II-stimulated tyrosine phosphorylation of Src and Cas and activation of ERK1/2 and JNK, but not p38, were potently inhibited by Src family tyrosine kinase inhibitors, herbimycin A (HA) and PP2. Ang II-stimulated Src and Cas association, tyrosine phosphorylation of Cas, and activation of ERK1/2 and JNK were suppressed in kinase-inactive Src (KI Src)-overexpressed RASMC. Ang II-stimulated JNK activation but not ERK1/2 activation was blocked in substrate domain-deleted Cas (DeltaSD Cas)-overexpressed RASMC. In addition, HA, PP2, ERK1/2 inhibitor, 2'-amino-3'-methoxyflavone (PD98059) and JNK inhibitor, and anthra[1,9-cd]pyrazol-6(2H)-one (SP600125) significantly inhibited Ang II-stimulated migration of RASMC. Ang II-induced colocalization of Src and Cas and migration were inhibited in both KI Src- and DeltaSD Cas-overexpressed RASMC. These findings suggest that Src and Cas are essentially but differentially involved in Ang II-stimulated migration of VSMC through the activation of ERK1/2 and JNK.","ja":"Angiotensin II (Ang II) plays an important role in several cardiovascular diseases associated with vascular smooth muscle cell (VSMC) growth and migration. Src activity is known to be required for the migration of a number of cell types. p130Cas was reported to be essential for cell migration and actin filament reorganization. Mitogen-activated protein (MAP) kinases were also reported to be critical regulatory factors for growth and migration of VSMC. However, precise intracellular mechanisms involving c-Src, p130Cas, and MAP kinases in Ang II-stimulated migration of VSMC have not been well elucidated. Here we demonstrated that Ang II rapidly and significantly stimulated tyrosine phosphorylation of Src and Cas and their association in rat aortic smooth muscle cells (RASMC). Ang II-stimulated tyrosine phosphorylation of Src and Cas and activation of ERK1/2 and JNK, but not p38, were potently inhibited by Src family tyrosine kinase inhibitors, herbimycin A (HA) and PP2. Ang II-stimulated Src and Cas association, tyrosine phosphorylation of Cas, and activation of ERK1/2 and JNK were suppressed in kinase-inactive Src (KI Src)-overexpressed RASMC. Ang II-stimulated JNK activation but not ERK1/2 activation was blocked in substrate domain-deleted Cas (DeltaSD Cas)-overexpressed RASMC. In addition, HA, PP2, ERK1/2 inhibitor, 2'-amino-3'-methoxyflavone (PD98059) and JNK inhibitor, and anthra[1,9-cd]pyrazol-6(2H)-one (SP600125) significantly inhibited Ang II-stimulated migration of RASMC. Ang II-induced colocalization of Src and Cas and migration were inhibited in both KI Src- and DeltaSD Cas-overexpressed RASMC. These findings suggest that Src and Cas are essentially but differentially involved in Ang II-stimulated migration of VSMC through the activation of ERK1/2 and JNK."},"publication_date":"2004-04","publication_name":{"en":"Molecular Pharmacology","ja":"Molecular Pharmacology"},"volume":"Vol.65","number":"No.4","starting_page":"832","ending_page":"841","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1124/mol.65.4.832"],"issn":["0026-895X"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:83, {"insert":{"user_id":"B000337971","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/14720501","label":"url"},{"@id":"https://cir.nii.ac.jp/crid/1571980076667609856/","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=90488","label":"url"}],"paper_title":{"en":"Ebselen inhibits tumor necrosis factor-α-induced c-jun N-terminal kinase activation and adhesion molecule expression in endothelial cells","ja":"Ebselen inhibits tumor necrosis factor-α-induced c-jun N-terminal kinase activation and adhesion molecule expression in endothelial cells"},"authors":{"en":[{"name":"Yoshizumi Masanori"},{"name":"Fujita Yoshiko"},{"name":"Izawa Yuki"},{"name":"Suzaki Yuki"},{"name":"Kyaw Moe"},{"name":"Ali Nermin"},{"name":"Tsuchiya Koichiro"},{"name":"Kagami Shoji"},{"name":"Yano Seiji"},{"name":"Sone Saburo"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"吉栖 正典"},{"name":"藤田 佳子"},{"name":"井澤 有紀"},{"name":"須崎 友紀"},{"name":"モーチョー"},{"name":"ネルミン アリ"},{"name":"土屋 浩一郎"},{"name":"香美 祥二"},{"name":"矢野 聖二"},{"name":"曽根 三郎"},{"name":"玉置 俊晃"}]},"description":{"en":"Tumor necrosis factor-alpha (TNF-alpha) stimulates expression of endothelial cell (EC) genes that may promote atherosclerosis in part by an activation of mitogen-activated protein (MAP) kinases. Ebselen (2-phenyl-1,2-benzisoselenazol-3[2H]-one), a selenoorganic compound, is effective for acute ischemic stroke; however, its effect on EC has not yet been elucidated. We examined the effect of ebselen on TNF-alpha-induced MAP kinase activation and adhesion molecule expression in cultured human umbilical vein endothelial cells (HUVEC). Extracellular signal-regulated kinase (ERK1/2), c-Jun N-terminal kinase (JNK) and p38 were rapidly and significantly activated by TNF-alpha in HUVEC. TNF-alpha-induced JNK activation was inhibited by ebselen, whereas ERK1/2 and p38 were not affected. Apoptosis signal-regulated kinase 1 (ASK1) was suggested to be involved in TNF-alpha-induced JNK activation because transfection of kinase-inactive ASK1 inhibited TNF-alpha-induced JNK activation. Ebselen inhibited TNF-alpha-induced TNF receptor-associated factor 2 (TRAF2)-ASK1 complex formation and phosphorylation of stress-activated protein kinase ERK kinase 1 (SEK1), which is an upstream signaling molecule of JNK. Finally, TNF-alpha-induced activator protein-1 (AP-1) and nuclear factor-kappaB (NF-kappaB) activation and resultant intracellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) expressions were inhibited by ebselen. Specific inhibitors for JNK and NF-kappaB also inhibited TNF-alpha-induced ICAM-1 and VCAM-1 expressions in HUVEC. These findings suggest that ebselen prevents TNF-alpha-induced EC activation through the inhibition of TRAF2-ASK1-SEK1 signaling pathway, which leads to JNK activation. Inhibition of JNK by ebselen may imply its usefulness for the prevention of atherosclerosis relevant to EC activation.","ja":"Tumor necrosis factor-alpha (TNF-alpha) stimulates expression of endothelial cell (EC) genes that may promote atherosclerosis in part by an activation of mitogen-activated protein (MAP) kinases. Ebselen (2-phenyl-1,2-benzisoselenazol-3[2H]-one), a selenoorganic compound, is effective for acute ischemic stroke; however, its effect on EC has not yet been elucidated. We examined the effect of ebselen on TNF-alpha-induced MAP kinase activation and adhesion molecule expression in cultured human umbilical vein endothelial cells (HUVEC). Extracellular signal-regulated kinase (ERK1/2), c-Jun N-terminal kinase (JNK) and p38 were rapidly and significantly activated by TNF-alpha in HUVEC. TNF-alpha-induced JNK activation was inhibited by ebselen, whereas ERK1/2 and p38 were not affected. Apoptosis signal-regulated kinase 1 (ASK1) was suggested to be involved in TNF-alpha-induced JNK activation because transfection of kinase-inactive ASK1 inhibited TNF-alpha-induced JNK activation. Ebselen inhibited TNF-alpha-induced TNF receptor-associated factor 2 (TRAF2)-ASK1 complex formation and phosphorylation of stress-activated protein kinase ERK kinase 1 (SEK1), which is an upstream signaling molecule of JNK. Finally, TNF-alpha-induced activator protein-1 (AP-1) and nuclear factor-kappaB (NF-kappaB) activation and resultant intracellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) expressions were inhibited by ebselen. Specific inhibitors for JNK and NF-kappaB also inhibited TNF-alpha-induced ICAM-1 and VCAM-1 expressions in HUVEC. These findings suggest that ebselen prevents TNF-alpha-induced EC activation through the inhibition of TRAF2-ASK1-SEK1 signaling pathway, which leads to JNK activation. Inhibition of JNK by ebselen may imply its usefulness for the prevention of atherosclerosis relevant to EC activation."},"publication_date":"2004-03","publication_name":{"en":"Experimental Cell Research","ja":"Experimental Cell Research"},"volume":"Vol.292","number":"No.1","starting_page":"1","ending_page":"10","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1016/j.yexcr.2003.08.003"],"issn":["0014-4827"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:84, {"insert":{"user_id":"B000337971","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/14757132","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=113753","label":"url"}],"paper_title":{"en":"Ebsalen inhibits p38MAP kinase-mediated endothelial cell death by hydrogen peroxide.","ja":"Ebsalen inhibits p38MAP kinase-mediated endothelial cell death by hydrogen peroxide."},"authors":{"en":[{"name":"Ali Nermin"},{"name":"Yoshizumi Masanori"},{"name":"Tsuchiya Koichiro"},{"name":"Kyaw Moe"},{"name":"Fujita Yoshiko"},{"name":"Izawa Yuki"},{"name":"Abe Shinji"},{"name":"Kanematsu Yasuhisa"},{"name":"Kagami Shoji"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"Ali Nermin"},{"name":"吉栖 正典"},{"name":"土屋 浩一郎"},{"name":"Kyaw Moe"},{"name":"藤田 佳子"},{"name":"井澤 有紀"},{"name":"阿部 真治"},{"name":"兼松 康久"},{"name":"香美 祥二"},{"name":"玉置 俊晃"}]},"description":{"en":"Ebselen (2-phenyl-1, 2-benzisoselenazol-3[2H]-one) is a seleno-organic compound exhibiting both glutathione peroxidase and antioxidant activity. Although it has been reported that ebselen is effective against hydrogen peroxide (H(2)O(2))-induced cell death in several cell types, its effect on endothelial cell damage has not yet been elucidated. In the present study, we examined the effect of ebselen on H(2)O(2)-induced human umbilical vein endothelial cells (HUVECs) death, and its intracellular mechanism. Our findings showed that pretreatment of HUVECs with ebselen resulted in a significant recovery from H(2)O(2)-induced cell death in a concentration-dependent manner. In addition to the inhibition of lactate dehydrogenase (LDH) leakage, ebselen inhibited H(2)O(2)-induced cytochrome c release and caspase-3 activation and the resultant apoptosis in HUVECs. Moreover, it was observed that H(2)O(2) significantly stimulated activation of mitogen-activated protein (MAP) kinases, i.e., p38 MAP kinase, c-Jun N-terminal kinase (JNK) and extracellular signal-regulated kinase (ERK1/2). Ebselen inhibited H(2)O(2)-induced p38 MAP kinase, but not JNK or ERK1/2 activation. Furthermore, SB203580 (4-[4-fluorophenyl]-2-[4-methylsulfinylphenyl]-5-[4-pyridyl]-1H-imidazole), a specific p38 MAP kinase inhibitor, inhibited H(2)O(2)-induced p38 MAP kinase phosphorylation, cytochrome c release, caspase-3 activation, as well as cell death in HUVECs. These findings suggest that ebselen attenuates H(2)O(2)-induced endothelial cell death through the inhibition of signaling pathways mediated by p38 MAP kinase, caspase-3, and cytochrome c release. Thus, inhibition of p38 MAP kinase by ebselen may imply its usefulness for prevention and/or treatment of endothelial cell dysfunction, which was suggested to be the first step in the development of atherosclerosis.","ja":"Ebselen (2-phenyl-1, 2-benzisoselenazol-3[2H]-one) is a seleno-organic compound exhibiting both glutathione peroxidase and antioxidant activity. Although it has been reported that ebselen is effective against hydrogen peroxide (H(2)O(2))-induced cell death in several cell types, its effect on endothelial cell damage has not yet been elucidated. In the present study, we examined the effect of ebselen on H(2)O(2)-induced human umbilical vein endothelial cells (HUVECs) death, and its intracellular mechanism. Our findings showed that pretreatment of HUVECs with ebselen resulted in a significant recovery from H(2)O(2)-induced cell death in a concentration-dependent manner. In addition to the inhibition of lactate dehydrogenase (LDH) leakage, ebselen inhibited H(2)O(2)-induced cytochrome c release and caspase-3 activation and the resultant apoptosis in HUVECs. Moreover, it was observed that H(2)O(2) significantly stimulated activation of mitogen-activated protein (MAP) kinases, i.e., p38 MAP kinase, c-Jun N-terminal kinase (JNK) and extracellular signal-regulated kinase (ERK1/2). Ebselen inhibited H(2)O(2)-induced p38 MAP kinase, but not JNK or ERK1/2 activation. Furthermore, SB203580 (4-[4-fluorophenyl]-2-[4-methylsulfinylphenyl]-5-[4-pyridyl]-1H-imidazole), a specific p38 MAP kinase inhibitor, inhibited H(2)O(2)-induced p38 MAP kinase phosphorylation, cytochrome c release, caspase-3 activation, as well as cell death in HUVECs. These findings suggest that ebselen attenuates H(2)O(2)-induced endothelial cell death through the inhibition of signaling pathways mediated by p38 MAP kinase, caspase-3, and cytochrome c release. Thus, inhibition of p38 MAP kinase by ebselen may imply its usefulness for prevention and/or treatment of endothelial cell dysfunction, which was suggested to be the first step in the development of atherosclerosis."},"publication_date":"2004-02-06","publication_name":{"en":"European Journal of Pharmacology","ja":"European Journal of Pharmacology"},"volume":"Vol.485","number":"No.1-3","starting_page":"127","ending_page":"135","languages":["eng"],"referee":true,"identifiers":{"doi":["10.1016/j.ejphar.2003.11.079"],"issn":["0014-2999"]},"published_paper_type":"scientific_journal"},"priority":"input_data"}
line:85, {"insert":{"user_id":"B000337971","type":"published_papers","id":"39666257"},"force":{"see_also":[{"@id":"http://repo.lib.tokushima-u.ac.jp/116860","label":"url"},{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/116860","label":"url"},{"@id":"https://cir.nii.ac.jp/crid/1050010293735891072/","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=390120","label":"url"}],"paper_title":{"en":"研究に関する男女共同参画・ダイバーシティの推進状況に関するアンケート調査-全国の集計結果との比較から見える徳島大学の現状-","ja":"研究に関する男女共同参画・ダイバーシティの推進状況に関するアンケート調査-全国の集計結果との比較から見える徳島大学の現状-"},"authors":{"en":[{"name":"Izawa-Ishizawa Yuki"},{"name":"Bando Yoshimi"},{"name":"Sumitani Satsuki"},{"name":"Tangoku Akira"},{"name":"Haku Mari"}],"ja":[{"name":"石澤 有紀"},{"name":"坂東 良美"},{"name":"住谷 さつき"},{"name":"丹黒 章"},{"name":"葉久 真理"}]},"description":{"en":"本調査では，全国ダイバーシティネットワークの幹事機関である大阪大学と，日本学術会議科学者委員会男女共同参画分科会・同アンケート検討小分科会が共同で実施した「大学・研究機関における男女共同参画・ダイバーシティの推進状況調査」のうち「大学・研究機関における男女共同参画の推進状況に対する意見・感想」について，徳島大学回答分(男性60 件，女性21 件)のみ抽出されたデータを用いて，本学における男女共同参画・ダイバーシティ推進に関する研究者の意識調査を実施した．男女別に集計し，公開されている全国集計結果(計10，105 件)と比較検討することで，全国における本学の位置付けについて分析した． 調査項目は， 1 ．男女共同参画の推進(全般) 2 ．男女共同参画の取り組み 3 ．ワークライフバランス・育児支援サービス 4 ．ダイバーシティ対応 5 ．ハラスメント防止体制 6 ．医学系 の6 項目にわたる．全国と徳島での回答差，また男女間の回答差から，現在の徳島大学の研究者における男女共同参画に対する意識について考察する．","ja":"本調査では，全国ダイバーシティネットワークの幹事機関である大阪大学と，日本学術会議科学者委員会男女共同参画分科会・同アンケート検討小分科会が共同で実施した「大学・研究機関における男女共同参画・ダイバーシティの推進状況調査」のうち「大学・研究機関における男女共同参画の推進状況に対する意見・感想」について，徳島大学回答分(男性60 件，女性21 件)のみ抽出されたデータを用いて，本学における男女共同参画・ダイバーシティ推進に関する研究者の意識調査を実施した．男女別に集計し，公開されている全国集計結果(計10，105 件)と比較検討することで，全国における本学の位置付けについて分析した． 調査項目は， 1 ．男女共同参画の推進(全般) 2 ．男女共同参画の取り組み 3 ．ワークライフバランス・育児支援サービス 4 ．ダイバーシティ対応 5 ．ハラスメント防止体制 6 ．医学系 の6 項目にわたる．全国と徳島での回答差，また男女間の回答差から，現在の徳島大学の研究者における男女共同参画に対する意識について考察する．"},"publication_date":"2022-03","publication_name":{"en":"徳島大学人と地域共創センター紀要","ja":"徳島大学人と地域共創センター紀要"},"volume":"Vol.31","starting_page":"17","ending_page":"32","languages":["jpn"],"identifiers":{"issn":["2435-1822"]},"published_paper_type":"research_institution"},"priority":"input_data"}
line:86, {"insert":{"user_id":"B000337971","type":"published_papers"},"similar_merge":{"see_also":[{"@id":"http://ci.nii.ac.jp/naid/40007059225/","label":"url"},{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/47262","label":"url"},{"@id":"https://cir.nii.ac.jp/crid/1050845762393810304/","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=131150","label":"url"}],"paper_title":{"en":"Lysophosphatidylcholine(LPC)transactivates vascular endothelial growth factor(VEGF) receptor via c-Src in HUVEC","ja":"ヒト臍帯静脈内皮細胞(HUVEC)における Lysophosphatidylcholine(LPC)刺激によるVEGFレセプターのトランスアクチベーション"},"authors":{"en":[{"name":"Fujita Yoshiko"},{"name":"Yoshizumi Masanori"},{"name":"Izawa Yuki"},{"name":"Kanematsu Yasuhisa"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"藤田 佳子"},{"name":"吉栖 正典"},{"name":"井澤 有紀"},{"name":"兼松 康久"},{"name":"玉置 俊晃"}]},"description":{"en":"One of the major lipid components of oxidized low density lipoprotein, lysophosphatidylcholine(LPC)is involved in numerous biological processes as a bioactive lipid molecule and has beenshown to be involved in the progression of atherosclerosis. As counter-ligands, G2A and GPR4wereidentified with high binding affinity for LPC that are belonging to orphan G-protein-coupledreceptors(GPCRs)at plasma membranes. Although several GPCR ligands transactivate receptortyrosine kinases (RTKs), such as epidermal growth factor receptor, transactivation of RTK byLPC has not yet been reported. Here we observed for the first time that LPC treatment inducestyrosyl phosphorylation of vascular endothelial growth factor(VEGF)receptor2(fetal liverkinase-1/kinase-insert domain-containing receptor, Flk-1/KDR)in human umbilical vein endothelialcells(HUVEC). VEGF receptor tyrosine kinase inhibitors, SU1498and VTKi inhibited Flk-1/KDRtransactivation by LPC. Furthermore, we examined the effect of the Src family kinases inhibitors,Herbimycin A and PP2 on LPC-induced Flk-1/KDR transactivation. Herbimycin A and PP2inhibited Flk-1/KDR transactivation in HUVEC, suggesting that c-Src is involved in LPC-inducedFlk-1/KDR transactivation. Kinase-inactive(KI)Src transfection also inhibited LPC-induced Flk-1/KDR transactivation. In addition, LPC activated extracellular signal-regulated kinase1/2and Akt,which are downstream effectors of Flk-1/KDR, and these were inhibited by SU1498，VTKi,Herbimycin A, PP2and KI Src transfection in HUVEC. LPC-mediated HUVEC proliferation wasshown to be secondary to transactivation because it was suppressed by SU1498，VTKi, HerbimycinA, PP2and KI Src transfection. It is concluded that c-Src-mediated Flk-1/KDR transactivation byLPC may have important implications for the progression of atherosclerosis.","ja":"One of the major lipid components of oxidized low density lipoprotein, lysophosphatidylcholine(LPC)is involved in numerous biological processes as a bioactive lipid molecule and has beenshown to be involved in the progression of atherosclerosis. As counter-ligands, G2A and GPR4wereidentified with high binding affinity for LPC that are belonging to orphan G-protein-coupledreceptors(GPCRs)at plasma membranes. Although several GPCR ligands transactivate receptortyrosine kinases (RTKs), such as epidermal growth factor receptor, transactivation of RTK byLPC has not yet been reported. Here we observed for the first time that LPC treatment inducestyrosyl phosphorylation of vascular endothelial growth factor(VEGF)receptor2(fetal liverkinase-1/kinase-insert domain-containing receptor, Flk-1/KDR)in human umbilical vein endothelialcells(HUVEC). VEGF receptor tyrosine kinase inhibitors, SU1498and VTKi inhibited Flk-1/KDRtransactivation by LPC. Furthermore, we examined the effect of the Src family kinases inhibitors,Herbimycin A and PP2 on LPC-induced Flk-1/KDR transactivation. Herbimycin A and PP2inhibited Flk-1/KDR transactivation in HUVEC, suggesting that c-Src is involved in LPC-inducedFlk-1/KDR transactivation. Kinase-inactive(KI)Src transfection also inhibited LPC-induced Flk-1/KDR transactivation. In addition, LPC activated extracellular signal-regulated kinase1/2and Akt,which are downstream effectors of Flk-1/KDR, and these were inhibited by SU1498，VTKi,Herbimycin A, PP2and KI Src transfection in HUVEC. LPC-mediated HUVEC proliferation wasshown to be secondary to transactivation because it was suppressed by SU1498，VTKi, HerbimycinA, PP2and KI Src transfection. It is concluded that c-Src-mediated Flk-1/KDR transactivation byLPC may have important implications for the progression of atherosclerosis."},"publication_date":"2005-08-25","publication_name":{"en":"Shikoku Acta Medica","ja":"四国医学雑誌"},"volume":"Vol.61","number":"No.3,4","starting_page":"91","ending_page":"94","languages":["jpn"],"identifiers":{"issn":["0037-3699"]},"published_paper_type":"research_institution"},"priority":"input_data"}
line:87, {"insert":{"user_id":"B000337971","type":"published_papers","id":"36014070"},"force":{"see_also":[{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/116895","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=383376","label":"url"}],"paper_title":{"en":"Drug-Repositioning Approaches Based on Medical and Life Science Databases.","ja":"Drug-Repositioning Approaches Based on Medical and Life Science Databases."},"authors":{"en":[{"name":"Zamami Yoshito"},{"name":"Hamano Hirofumi"},{"name":"Niimura Takahiro"},{"name":"Aizawa Fuka"},{"name":"Yagi Kenta"},{"name":"Goda Mitsuhiro"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"座間味 義人"},{"name":"濱野 裕章"},{"name":"新村 貴博"},{"name":"相澤 風花"},{"name":"八木 健太"},{"name":"合田 光寛"},{"name":"石澤 有紀"},{"name":"石澤 啓介"}]},"publication_date":"2021-11-01","publication_name":{"en":"Frontiers in Pharmacology","ja":"Frontiers in Pharmacology"},"volume":"Vol.12","number":"No.752174","languages":["eng"],"identifiers":{"doi":["10.3389/fphar.2021.752174"],"issn":["1663-9812"]}},"priority":"input_data"}
==== end registerFile(/WWW/pub2/data/ERD/person/229223/researchmap/published_papers.jsonl, _j7NNpMBwbWENEENUzCR) ====
==== begin registerFile(/WWW/pub2/data/ERD/person/229223/researchmap/misc.jsonl) ====
line:1, {"insert":{"user_id":"B000337971","type":"misc"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/38432934","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=406561","label":"url"}],"paper_title":{"en":"[Development of Preventive Methods for Drug-induced Cardiotoxicity Using a Large-scale Medical Information Database].","ja":"[Development of Preventive Methods for Drug-induced Cardiotoxicity Using a Large-scale Medical Information Database]."},"authors":{"en":[{"name":"Hamano Hirofumi"},{"name":"Zamami Yoshito"},{"name":"Ushio Soichiro"},{"name":"Niimura Takahiro"},{"name":"Goda Mitsuhiro"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Ishizawa Keisuke"}],"ja":[{"name":"濱野 裕章"},{"name":"座間味 義人"},{"name":"Ushio Soichiro"},{"name":"新村 貴博"},{"name":"合田 光寛"},{"name":"石澤 有紀"},{"name":"石澤 啓介"}]},"description":{"en":"Cancer therapies have evolved considerably thereby substantially improving the survival of patients with cancer. However, cardiotoxicity, such as myocarditis and heart failure, induced by anticancer drugs, including immune checkpoint inhibitor(ICI)s and doxorubicin, present serious challenges. Numerous observations have indicated increased risks of cardiotoxicity- and cancer-related mortality in patients with drug-induced cardiotoxicity. Therefore, the prevention and management of drug-induced cardiotoxicity should be prioritized to enable sustainable long-term treatment while preserving patients' quality of life. Recently, medical research has been primarily focused on elucidation of therapeutic benefits and adverse events using medical big data, including worldwide databases of adverse events. The aim of the present study was to establish prevention strategies for drug-induced cardiotoxicity and advance data analytics. A data-driven approach was adopted to comprehensively analyze patient data and drug-induced cardiotoxicity. These data analytics revealed numerous risk factors, leading to the development of drugs that mitigate these factors. Furthermore, many unknown adverse events with molecularly targeted drugs were brought to light. Consequently, the importance of managing adverse events, guided by insights from data science, is predicted to increase. In this symposium review, we introduce our research exemplifying pharmaceutical studies utilizing medical big data. In particular, we discuss in detail the risk factors associated with myocarditis induced by immune checkpoint inhibitors along with prophylactic agents to mitigate doxorubicin-induced cardiotoxicity.","ja":"Cancer therapies have evolved considerably thereby substantially improving the survival of patients with cancer. However, cardiotoxicity, such as myocarditis and heart failure, induced by anticancer drugs, including immune checkpoint inhibitor(ICI)s and doxorubicin, present serious challenges. Numerous observations have indicated increased risks of cardiotoxicity- and cancer-related mortality in patients with drug-induced cardiotoxicity. Therefore, the prevention and management of drug-induced cardiotoxicity should be prioritized to enable sustainable long-term treatment while preserving patients' quality of life. Recently, medical research has been primarily focused on elucidation of therapeutic benefits and adverse events using medical big data, including worldwide databases of adverse events. The aim of the present study was to establish prevention strategies for drug-induced cardiotoxicity and advance data analytics. A data-driven approach was adopted to comprehensively analyze patient data and drug-induced cardiotoxicity. These data analytics revealed numerous risk factors, leading to the development of drugs that mitigate these factors. Furthermore, many unknown adverse events with molecularly targeted drugs were brought to light. Consequently, the importance of managing adverse events, guided by insights from data science, is predicted to increase. In this symposium review, we introduce our research exemplifying pharmaceutical studies utilizing medical big data. In particular, we discuss in detail the risk factors associated with myocarditis induced by immune checkpoint inhibitors along with prophylactic agents to mitigate doxorubicin-induced cardiotoxicity."},"publication_date":"2024","publication_name":{"en":"Journal of the Pharmaceutical Society of Japan","ja":"薬学雑誌"},"volume":"Vol.144","number":"No.3","starting_page":"257","ending_page":"264","languages":["jpn"],"identifiers":{"doi":["10.1248/yakushi.23-00164-2"],"issn":["1347-5231"]},"misc_type":"introduction_scientific_journal"},"priority":"input_data"}
line:2, {"insert":{"user_id":"B000337971","type":"misc"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/24882646","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=278303","label":"url"}],"paper_title":{"en":"Drug development for cardiorenal disease based on oxidative stress control","ja":"酸化ストレス制御を基盤とする新規心腎血管障害治療薬の開発"},"authors":{"en":[{"name":"Imanishi Masaki"},{"name":"Ishizawa Keisuke"},{"name":"SAKURADA TAKUMI"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Yamano Noriko"},{"name":"Kihira Yoshitaka"},{"name":"Ikeda Yasumasa"},{"name":"Tsuchiya Koichiro"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"今西 正樹"},{"name":"石澤 啓介"},{"name":"櫻田 巧"},{"name":"石澤 有紀"},{"name":"山野 範子"},{"name":"木平 孝高"},{"name":"池田 康将"},{"name":"土屋 浩一郎"},{"name":"玉置 俊晃"}]},"description":{"en":"Oxidative stress is a key factor involved in the pathogenesis and progression of cardiovascular disease (CVD) and chronic kidney disease (CKD). Reactive oxygen species (ROS), produced as a result of redox reactions in various cells, have been recognized as key chemical mediators causing cellular damage and organ dysfunction in CVD and CKD. Nifedipine, a well-known calcium channel blocker, is extremely sensitive to light which gets converted to its nitroso analog, nitrosonifedipine (NO-NIF) in the presence of ultraviolet and visible light. The so formed NO-NIF blocks calcium channel quite weakly compared to that of nifedipine. However, we elucidated for the first time that NO-NIF is converted to NO-NIF radical which acquires extremely strong antioxidant property via reaction with unsaturated fatty acid or endothelial cells. We have already reported that NO-NIF reduces the cytotoxicity of cumene hydroperoxide, which hampers the integrity of cell membrane through oxidative stress, in endothelial cells. Additionally, we demonstrated that NO-NIF restored acetylcholine-responsive vascular relaxation and suppressed intercellular adhesion molecule-1 expression in the aorta of N(ω)-nitro-L-arginine methyl ester-treated rats, a model of vascular endothelial dysfunction. Recently, we reported that NO-NIF ameliorates angiotensin II-induced vascular remodeling via antioxidative effects in vivo and in vitro. These observations point towards the plausible, unique role of NO-NIF as a novel antioxidant which improves vascular dysfunction for overcoming CVD and CKD and the same has been highlighted in this review.","ja":"Oxidative stress is a key factor involved in the pathogenesis and progression of cardiovascular disease (CVD) and chronic kidney disease (CKD). Reactive oxygen species (ROS), produced as a result of redox reactions in various cells, have been recognized as key chemical mediators causing cellular damage and organ dysfunction in CVD and CKD. Nifedipine, a well-known calcium channel blocker, is extremely sensitive to light which gets converted to its nitroso analog, nitrosonifedipine (NO-NIF) in the presence of ultraviolet and visible light. The so formed NO-NIF blocks calcium channel quite weakly compared to that of nifedipine. However, we elucidated for the first time that NO-NIF is converted to NO-NIF radical which acquires extremely strong antioxidant property via reaction with unsaturated fatty acid or endothelial cells. We have already reported that NO-NIF reduces the cytotoxicity of cumene hydroperoxide, which hampers the integrity of cell membrane through oxidative stress, in endothelial cells. Additionally, we demonstrated that NO-NIF restored acetylcholine-responsive vascular relaxation and suppressed intercellular adhesion molecule-1 expression in the aorta of N(ω)-nitro-L-arginine methyl ester-treated rats, a model of vascular endothelial dysfunction. Recently, we reported that NO-NIF ameliorates angiotensin II-induced vascular remodeling via antioxidative effects in vivo and in vitro. These observations point towards the plausible, unique role of NO-NIF as a novel antioxidant which improves vascular dysfunction for overcoming CVD and CKD and the same has been highlighted in this review."},"publication_date":"2014-06","publication_name":{"en":"Journal of the Pharmaceutical Society of Japan","ja":"薬学雑誌"},"volume":"Vol.134","number":"No.6","starting_page":"715","ending_page":"719","languages":["jpn"],"identifiers":{"doi":["10.1248/yakushi.13-00255-4"],"issn":["1347-5231"]},"misc_type":"introduction_scientific_journal"},"priority":"input_data"}
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====== BulkResult(B000337971, Ez7NNpMBwbWENEENWDEz) : End ======