徳島大学 / 教育研究者総覧 --- 内田貴之

専門分野

研究テーマ

著書・論文

著書:

1.	内田貴之, 二川健 : 微小重力環境における筋萎縮発生メカニズムへの新展開, 北隆館, 東京, 2018年10月. (キーワード) ミトコンドリア (mitochondria) / 筋萎縮 (muscle atrophy)
2.	内田貴之, 二川健 : サルコペニア発症におけるメカニカルストレスの関与, 2016年4月. (キーワード) 筋肉 (muscle) / 酸化ストレス (oxidative stress)

学術論文(審査論文):

1.	Takayuki Uchida, Kohno Madoka, Chinami Itoh, Erika Yamano, Hiroki Matsuki, MIZANUR MD Rahman, ANAYT ULLA, Minori Suzuki, Takahiro Ishiguro and Takeshi Nikawa : Inhibitory Effect of Kori-tofu Protein on Denervation-Induced Atrogene Expression in Mouse Skeletal Muscle, Biological Sciences in Space, Vol.38, 1-7, 2024.
2.	Keisuke Ozaki, Tomoya Fukawa, Kei Daizumoto, Yutaro Sasaki, Yoshiteru Ueno, Megumi Tsuda, Takayuki Uchida, Yoshito Kusuhara, Yasuyo Yamamoto, Kunihisa Yamaguchi, Masayuki Takahashi and Hiro-omi Kanayama : The impact of nutritional status and changes of body composition on the prognosis of metastatic renal cell carcinoma patients., The Journal of Medical Investigation : JMI, Vol.70, No.1.2, 80-87, 2023. (要約) Nutritional status of mRCC patients may predict changes in body composition and be associated with their prognosis. J. Med. Invest. 70 : 80-87, February, 2023. (キーワード) Humans / Carcinoma, Renal Cell / Kidney Neoplasms / Nutritional Status / Prognosis / Body Composition / Retrospective Studies / Protein Kinase Inhibitors (徳島大学機関リポジトリ) ● Metadata: 118311 (出版サイトへのリンク) ● Publication site (DOI): 10.2152/jmi.70.80 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37164748 ● Search Scopus @ Elsevier (PMID): 37164748 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.70.80 (徳島大学機関リポジトリ: 118311, DOI: 10.2152/jmi.70.80, PubMed: 37164748)
3.	ANAYT ULLA, Kanae Osaki, Mizanur Md Rahman, Reiko Nakao, Takayuki Uchida, Isafumi Maru, Kazuaki Mawatari, Tomoya Fukawa, Hiro-omi Kanayama, Iori Sakakibara, Katsuya Hirasaka and Takeshi Nikawa : Morin improves dexamethasone-induced muscle atrophy by modulating atrophy-related genes and oxidative stress in female mice., Bioscience, Biotechnology, and Biochemistry, Vol.86, No.10, 1448-1458, 2022. (要約) This study investigated the effect of morin, a flavonoid, on dexamethasone-induced muscle atrophy in C57BL/6J female mice. Dexamethasone (10 mg/kg body weight) for 10 days significantly reduced body weight, gastrocnemius and tibialis anterior muscle mass, and muscle protein in mice. Dexamethasone significantly upregulated muscle atrophy-associated ubiquitin ligases, including atrogin-1 and MuRF-1, and the upstream transcription factors FoxO3a and Klf15. Additionally, dexamethasone significantly induced the expression of oxidative stress-sensitive ubiquitin ligase Cbl-b and the accumulation of the oxidative stress markers malondialdehyde and advanced protein oxidation products in both the plasma and skeletal muscle samples. Intriguingly, morin treatment (20 mg/kg body weight) for 17 days effectively attenuated the loss of muscle mass and muscle protein and suppressed the expression of ubiquitin ligases while reducing the expression of upstream transcriptional factors. Therefore, morin might act as a potential therapeutic agent to attenuate muscle atrophy by modulating atrophy-inducing genes and preventing oxidative stress. (キーワード) Animals / Body Weight / Dexamethasone / Female / Flavones / Malondialdehyde / Mice / Mice, Inbred C57BL / Muscle Proteins / Muscle, Skeletal / Muscular Atrophy / Oxidative Stress / Tripartite Motif Proteins / Ubiquitin-Protein Ligases (出版サイトへのリンク) ● Publication site (DOI): 10.1093/bbb/zbac140 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35977398 ● Search Scopus @ Elsevier (PMID): 35977398 ● Search Scopus @ Elsevier (DOI): 10.1093/bbb/zbac140 (DOI: 10.1093/bbb/zbac140, PubMed: 35977398)
4.	Yuichiro Adachi, Masashi Masuda, Iori Sakakibara, Takayuki Uchida, Yuki Niida, Yuki Mori, Yuki Kamei, Yosuke Okumura, Hirokazu Ohminami, Kohta Ohnishi, Hisami Okumura, Takeshi Nikawa and Yutaka Taketani : All-trans retinoic acid changes muscle fiber type via increasing GADD34 dependent on MAPK signal., Life Science Alliance, Vol.5, No.7, 2022. (要約) All-trans retinoic acid (ATRA) increases the sensitivity to unfolded protein response in differentiating leukemic blasts. The downstream transcriptional factor of PERK, a major arm of unfolded protein response, regulates muscle differentiation. However, the role of growth arrest and DNA damage-inducible protein 34 (GADD34), one of the downstream factors of PERK, and the effects of ATRA on GADD34 expression in muscle remain unclear. In this study, we identified ATRA increased the GADD34 expression independent of the PERK signal in the gastrocnemius muscle of mice. ATRA up-regulated GADD34 expression through the transcriptional activation of gene via inhibiting the interaction of homeobox Six1 and transcription co-repressor TLE3 with the MEF3-binding site on the gene promoter in skeletal muscle. ATRA also inhibited the interaction of TTP, which induces mRNA degradation, with AU-rich element on mRNA via p-38 MAPK, resulting in the instability of mRNA. Overexpressed GADD34 in C2C12 cells changes the type of myosin heavy chain in myotubes. These results suggest ATRA increases GADD34 expression via transcriptional and post-transcriptional regulation, which changes muscle fiber type. (キーワード) Animals / Gene Expression Regulation / MAP Kinase Signaling System / Mice / Muscle Fibers, Skeletal / Protein Phosphatase 1 / RNA, Messenger / Transcription Factors / Tretinoin (徳島大学機関リポジトリ) ● Metadata: 117429 (出版サイトへのリンク) ● Publication site (DOI): 10.26508/lsa.202101345 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35318262 ● Search Scopus @ Elsevier (PMID): 35318262 ● Search Scopus @ Elsevier (DOI): 10.26508/lsa.202101345 (徳島大学機関リポジトリ: 117429, DOI: 10.26508/lsa.202101345, PubMed: 35318262)
5.	Kitahata Kanako, Takayuki Uchida, Taniguchi Runa, Kato Ayano, Kosuke Sugiura, Iori Sakakibara, Oarada Motoko, Tomoya Fukawa, Junsoo Park, Inho Choi and Takeshi Nikawa : Additional effects of simultaneous treatment with C14-Cblin and celastrol on the clinorotation-induced rat L6 myotube atrophy, The Journal of Medical Investigation : JMI, Vol.69, No.1,2, 127-134, 2022. (要約) Two novel reagents, N-myristoylated Cbl-b inhibitory peptide (C14-Cblin) and celastrol, a quinone methide triterpene, are reported to be effective in preventing myotube atrophy. The combined effects of C14-Cblin and celastrol on rat L6 myotubes atrophy induced by 3D-clinorotation, a simulated microgravity model, was investigated in the present study. We first examined their effects on expression in atrogenes. Increase in MAFbx1/atrogin-1 and MuRF-1 by 3D-clinorotation was significantly suppressed by treatment with C14-Cblin or celastrol, but there was no additive effect of simultaneous treatment. However, celastrol significantly suppressed the upregulation of Cbl-b and HSP70 by 3D-clinorotation. Whereas 3D-clinorotation decreased the protein level of IRS-1 in L6 myotubes, C14-Cblin and celastrol inhibited the degradation of IRS-1. C14-Cblin and celastrol promoted the phosphorylation of FOXO3a even in microgravity condition. Simultaneous administration of C14-Cblin and celastrol had shown little additive effect in reversing the impairment of IGF-1 signaling by 3D-clinorotation. While 3D-clinorotation-induced marked oxidative stress in L6 myotubes, celastrol suppressed 3D-clinorotation-induced ROS production. Finally, the C14-Cblin and celastrol-treated groups were inhibited decrease in L6 myotube diameter and increased the protein content of slow-twitch MyHC cultured under 3D-clinorotation. The simultaneous treatment of C14-Cblin and celastrol additively prevented 3D-clinorotation-induced myotube atrophy than single treatment. J. Med. Invest. 69 : 127-134, February, 2022. (キーワード) Animals / Atrophy / Humans / Muscle Fibers, Skeletal / Pentacyclic Triterpenes / Rats / Rotation (徳島大学機関リポジトリ) ● Metadata: 116937 (出版サイトへのリンク) ● Publication site (DOI): 10.2152/jmi.69.127 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35466134 ● Search Scopus @ Elsevier (PMID): 35466134 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.69.127 (徳島大学機関リポジトリ: 116937, DOI: 10.2152/jmi.69.127, PubMed: 35466134)
6.	Madoka Kohno, ANAYT ULLA, Rina Taniguchi, Akane Ohishi, Kako Hirayama, Yuma Takemura, Shoichiro Takao, Yuki Kanazawa, Yuki Matsumoto, Masafumi Harada, Tomoya Fukawa, Hiro-omi Kanayama, Takayuki Uchida, Toshio Suzuki and Takeshi Nikawa : Daily Dietary Supplementation with Steamed Soybean Improves Muscle Volume and Strength in Healthy People Lacking Exercise., Journal of Nutritional Science and Vitaminology, Vol.68, No.6, 521-526, 2022. (要約) Various dietary protein supplements are used by the elderly and bedridden to maintain their skeletal muscle mass and functions. High-quality proteins act as an anabolic driver and help to improve muscle strength and performance. Previously, we reported that soy protein significantly attenuates denervation-induced loss of muscle mass and myofiber cross sectional area in mice with inhibition of ubiquitination and degradation of IRS-1 in tibialis anterior muscle. It also increased muscle volume and strength in bedridden patients. In the present study, we investigated the effects of dietary soybean supplementation on muscle functions in taxi drivers lacking vigorous physical exercise. We conducted a case-control study on 25 healthy, male taxi drivers between the ages of 36 and 71 y performing minimal physical exercise. They were divided into two dietary groups: the soybean diet group (n=13) who ate daily meals (dinner) supplemented with 50 g of steamed soybean for 30 d and the control diet group (n=12) who received no soybean supplement. Next, we measured the muscle cross-sectional area (CSA) and muscle strength and function in both the groups before and after 30 d of soybean intake. The body weights of both diet groups did not differ significantly over time. However, after 30 d of soybean supplementation, the soybean-fed group developed significantly higher muscle CSA and grip strength compared to the control groups. In conclusion, dietary soybean supplementation improved muscle function in taxi drivers who lacked exercise. (キーワード) Male / Animals / Mice / Soybeans / Case-Control Studies / Muscle, Skeletal / Dietary Supplements / Muscle Strength / Dietary Proteins (出版サイトへのリンク) ● Publication site (DOI): 10.3177/jnsv.68.521 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36596550 ● Search Scopus @ Elsevier (PMID): 36596550 ● Search Scopus @ Elsevier (DOI): 10.3177/jnsv.68.521 (DOI: 10.3177/jnsv.68.521, PubMed: 36596550)
7.	Taku Fukushima, Miho Takata, Ayano Kato, Takayuki Uchida, Takeshi Nikawa and Iori Sakakibara : Transcriptome Analyses of In Vitro Exercise Models by Clenbuterol Supplementation or Electrical Pulse Stimulation, Applied Sciences, Vol.11, No.21, 10436, 2021. (徳島大学機関リポジトリ) ● Metadata: 117280 (出版サイトへのリンク) ● Publication site (DOI): 10.3390/app112110436 (文献検索サイトへのリンク) ● Search Scopus @ Elsevier (DOI): 10.3390/app112110436 (徳島大学機関リポジトリ: 117280, DOI: 10.3390/app112110436)
8.	Reiko Nakao, Shen Weilin, Shimajiri Yasuka, Kainou Kumiko, Sato Yuki, Ulla Anayt, Kohta Ohnishi, Ninomiya Miyuki, Ohno Ayako, Takayuki Uchida, Tanaka Mitsuru, Akama Kazuhito, Matsui Toshiro and Takeshi Nikawa : Oral intake of rice overexpressing ubiquitin ligase inhibitory pentapeptide prevents atrophy in denervated skeletal muscle, NPJ Science of Food, Vol.5, No.1, 25, 2021. (要約) We previously reported that intramuscular injections of ubiquitin ligase CBLB inhibitory pentapeptide (Cblin; Asp-Gly-pTyr-Met-Pro) restored lost muscle mass caused by sciatic denervation. Here, we detected Cblin on the basolateral side of Caco-2 cells after being placed on the apical side, and found that cytochalasin D, a tight junction opener, enhanced Cblin transport. Orally administered Cblin was found in rat plasma, indicating that intact Cblin was absorbed in vitro and in vivo. Furthermore, transgenic Cblin peptide-enriched rice (CbR) prevented the denervation-induced loss of muscle mass and the upregulation of muscle atrophy-related ubiquitin ligases in mice. These findings indicated that CbR could serve as an alternative treatment for muscle atrophy. (徳島大学機関リポジトリ) ● Metadata: 117588 (出版サイトへのリンク) ● Publication site (DOI): 10.1038/s41538-021-00108-0 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34504092 ● Search Scopus @ Elsevier (PMID): 34504092 ● Search Scopus @ Elsevier (DOI): 10.1038/s41538-021-00108-0 (徳島大学機関リポジトリ: 117588, DOI: 10.1038/s41538-021-00108-0, PubMed: 34504092)
9.	Kosuke Sugiura, Katsuya Hirasaka, Tasuku Maeda, Takayuki Uchida, Koji Kishimoto, Motoko Oarada, Siegfried Labeit, Anayt Ulla, Iori Sakakibara, Reiko Nakao, Koichi Sairyo and Takeshi Nikawa : MuRF1 deficiency prevents age-related fat weight gain, possibly through accumulation of PDK4 in skeletal muscle mitochondria in older mice, Journal of Orthopaedic Research, Vol.40, No.5, 1026-1038, 2021. (徳島大学機関リポジトリ) ● Metadata: 116581 (出版サイトへのリンク) ● Publication site (DOI): 10.1002/jor.25131 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34185335 ● Summary page in Scopus @ Elsevier: 2-s2.0-85109422486 (徳島大学機関リポジトリ: 116581, DOI: 10.1002/jor.25131, PubMed: 34185335, Elsevier: Scopus)
10.	Ulla Anayt, Takayuki Uchida, Miki Yukari, Kosuke Sugiura, Higashitani Atsushi, Kobayashi Takeshi, Ohno Ayako, Reiko Nakao, Katsuya Hirasaka, Iori Sakakibara and Takeshi Nikawa : Morin attenuates dexamethasone-mediated oxidative stress and atrophy in mouse C2C12 skeletal myotubes, Archives of Biochemistry and Biophysics, Vol.704, 108873, 2021. (要約) Glucocorticoids are the drugs most commonly used to manage inflammatory diseases. However, they are prone to inducing muscle atrophy by increasing muscle proteolysis and decreasing protein synthesis. Various studies have demonstrated that antioxidants can mitigate glucocorticoid-induced skeletal muscle atrophy. Here, we investigated the effect of a potent antioxidative natural flavonoid, morin, on the muscle atrophy and oxidative stress induced by dexamethasone (Dex) using mouse C2C12 skeletal myotubes. Dex (10 μM) enhanced the production of reactive oxygen species (ROS) in C2C12 myotubes via glucocorticoid receptor. Moreover, Dex administration reduced the diameter and expression levels of the myosin heavy chain protein in C2C12 myotubes, together with the upregulation of muscle atrophy-associated ubiquitin ligases, such as muscle atrophy F-box protein 1/atrogin-1, muscle ring finger protein-1, and casitas B-lineage lymphoma proto-oncogene-b. Dex also significantly decreased phosphorylated Foxo3a and increased total Foxo3a expression. Interestingly, Dex-induced ROS accumulation and Foxo3a expression were inhibited by morin (10 μM) pretreatment. Morin also prevented the Dex-induced reduction of myotube thickness, together with muscle protein degradation and suppression of the upregulation of atrophy-associated ubiquitin ligases. In conclusion, our results suggest that morin effectively prevents glucocorticoid-induced muscle atrophy by reducing oxidative stress. (キーワード) Animals / Cell Line / Dexamethasone / Dose-Response Relationship, Drug / Flavonoids / Mice / Muscle Fibers, Skeletal / Muscle Proteins / Muscular Atrophy / Oxidative Stress (徳島大学機関リポジトリ) ● Metadata: 116344 (出版サイトへのリンク) ● Publication site (DOI): 10.1016/j.abb.2021.108873 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33848514 ● Search Scopus @ Elsevier (PMID): 33848514 ● Search Scopus @ Elsevier (DOI): 10.1016/j.abb.2021.108873 (徳島大学機関リポジトリ: 116344, DOI: 10.1016/j.abb.2021.108873, PubMed: 33848514)
11.	Sun Luchuanyang, Miyaji Nobuyuki, Yang Min, Mills M Edward, Taniyama Shigeto, Takayuki Uchida, Takeshi Nikawa, Li Jifeng, Shi Jie, Tachibana Katsuyasu and Katsuya Hirasaka : Astaxanthin Prevents Atrophy in Slow Muscle Fibers by Inhibiting Mitochondrial Reactive Oxygen Species via a Mitochondria-Mediated Apoptosis Pathway, Nutrients, Vol.13, No.379, 2021. (要約) Astaxanthin (AX) is a carotenoid that exerts potent antioxidant activity and acts in the lipid bilayer. This study aimed to investigate the effects of AX on muscle-atrophy-mediated disturbance of mitochondria, which have a lipid bilayer. Tail suspension was used to establish a muscle-atrophied mouse model. AX diet fed to tail-suspension mice prevented loss of muscle weight, inhibited the decrease of myofiber size, and restrained the increase of hydrogen peroxide (HO) production in the soleus muscle. Additionally, AX improved downregulation of mitochondrial respiratory chain complexes I and III in the soleus muscle after tail suspension. Meanwhile, AX promoted mitochondrial biogenesis by upregulating the expressions of , , in the soleus muscle of tail-suspension mice. To confirm the AX phenotype in the soleus muscle, we examined its effects on mitochondria using Sol8 myotubes derived from the soleus muscle. We found that AX was preferentially detected in the mitochondrial fraction; it significantly suppressed mitochondrial reactive oxygen species (ROS) production in Sol8 myotubes. Moreover, AX inhibited the activation of caspase 3 via inhibiting the release of cytochrome c into the cytosol in antimycin A-treated Sol8 myotubes. These results suggested that AX protected the functional stability of mitochondria, alleviated mitochondrial oxidative stress and mitochondria-mediated apoptosis, and thus, prevented muscle atrophy. (キーワード) astaxanthin / ミトコンドリア (mitochondria) / 筋委縮 (muscle atrophy) / 酸化ストレス (oxidative stress) (徳島大学機関リポジトリ) ● Metadata: 116285 (出版サイトへのリンク) ● Publication site (DOI): 10.3390/nu13020379 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33530505 ● Summary page in Scopus @ Elsevier: 2-s2.0-85099928726 (徳島大学機関リポジトリ: 116285, DOI: 10.3390/nu13020379, PubMed: 33530505, Elsevier: Scopus)
12.	Ohno Ayako, Nobuo Maita, Tabata Takanori, Nagano Hikaru, Arita Kyohei, Ariyoshi Mariko, Takayuki Uchida, Reiko Nakao, Ulla Anayt, Kosuke Sugiura, Koji Kishimoto, Teshima-Kondo Shigetada, Okumura Yuushi and Takeshi Nikawa : Crystal structure of inhibitor-bound human MSPL that can activate high pathogenic avian influenza., Life Science Alliance, Vol.4, No.6, e202000849, 2021. (要約) Infection of certain influenza viruses is triggered when its HA is cleaved by host cell proteases such as proprotein convertases and type II transmembrane serine proteases (TTSP). HA with a monobasic motif is cleaved by trypsin-like proteases, including TMPRSS2 and HAT, whereas the multibasic motif found in high pathogenicity avian influenza HA is cleaved by furin, PC5/6, or MSPL. MSPL belongs to the TMPRSS family and preferentially cleaves [R/K]-K-K-R sequences. Here, we solved the crystal structure of the extracellular region of human MSPL in complex with an irreversible substrate-analog inhibitor. The structure revealed three domains clustered around the C-terminal α-helix of the SPD. The inhibitor structure and its putative model show that the P1-Arg inserts into the S1 pocket, whereas the P2-Lys and P4-Arg interacts with the Asp/Glu-rich 99-loop that is unique to MSPL. Based on the structure of MSPL, we also constructed a homology model of TMPRSS2, which is essential for the activation of the SARS-CoV-2 spike protein and infection. The model may provide the structural insight for the drug development for COVID-19. (キーワード) Animals / Birds / Crystallography, X-Ray / Humans / Influenza in Birds / Membrane Proteins / Orthomyxoviridae / Protein Conformation / Serine Endopeptidases (徳島大学機関リポジトリ) ● Metadata: 116821 (出版サイトへのリンク) ● Publication site (DOI): 10.26508/LSA.202000849 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33820827 ● Summary page in Scopus @ Elsevier: 2-s2.0-85103997820 (徳島大学機関リポジトリ: 116821, DOI: 10.26508/LSA.202000849, PubMed: 33820827, Elsevier: Scopus)
13.	Yuki Niida, Masashi Masuda, Yuichiro Adachi, Aika Yoshizawa, Hirokazu Ohminami, Yuki Mori, Kohta Ohnishi, Hisami Okumura, Takayuki Uchida, Takeshi Nikawa, Hironori Yamamoto, Makoto Miyazaki and Yutaka Taketani : Reduction of stearoyl-CoA desaturase (SCD) contributes muscle atrophy through the excess endoplasmic reticulum stress in chronic kidney disease, Journal of Clinical Biochemistry and Nutrition, Vol.67, No.2, 179-187, 2020. (要約) <p>Skeletal muscle atrophy is associated with mortality and poor prognosis in patients with chronic kidney disease (CKD). However, underlying mechanism by which CKD causes muscle atrophy has not been completely understood. The quality of lipids (lipoquality), which is defined as the functional features of diverse lipid species, has recently been recognized as the pathology of various diseases. In this study, we investigated the roles of the stearoyl-CoA desaturase (SCD), which catalyzes the conversion of saturated fatty acids into monounsaturated fatty acids, in skeletal muscle on muscle atrophy in CKD model animals. In comparison to control rats, CKD rats decreased the SCD activity and its gene expression in atrophic gastrocnemius muscle. Next, oleic acid blocked the reduction of the thickness of C2C12 myotubes and the increase of the endoplasmic reticulum stress induced by SCD inhibitor. Furthermore, endoplasmic reticulum stress inhibitor ameliorated CKD-induced muscle atrophy (the weakness of grip strength and the decrease of muscle fiber size of gastrocnemius muscle) in mice and the reduction of the thickness of C2C12 myotubes by SCD inhibitor. These results suggest that the repression of SCD activity causes muscle atrophy through excessive endoplasmic reticulum stress in CKD.</p> (キーワード) skeletal muscle atrophy / endoplasmic reticulum stress / chronic kidney disease / stearoyl-CoA desaturase / saturated fatty acid (徳島大学機関リポジトリ) ● Metadata: 114720 (出版サイトへのリンク) ● Publication site (DOI): 10.3164/jcbn.20-24 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33041516 ● CiNii @ 国立情報学研究所 (CRID): 1390566775163696384 ● Search Scopus @ Elsevier (PMID): 33041516 ● Search Scopus @ Elsevier (DOI): 10.3164/jcbn.20-24 (徳島大学機関リポジトリ: 114720, DOI: 10.3164/jcbn.20-24, PubMed: 33041516, CiNii: 1390566775163696384)
14.	Tomohiro Yoshimura, Kanae Saitoh, Luchuanyang Sun, Yao Wang, Shigeto Taniyama, Kenichi Yamaguchi, Takayuki Uchida, Tsutomu Ohkubo, Atsushi Higashitani, Takeshi Nikawa, Katsuyasu Tachibana and Katsuya Hirasaka : Morin suppresses cachexia-induced muscle wasting by binding to ribosomal protein S10 in carcinoma cells., Biochemical and Biophysical Research Communications, Vol.506, No.4, 773-779, 2018. (要約) Cachexia, observed in most cancer patients, is a syndrome that includes wasting of bodily energy reserves and is characterized by muscle atrophy and fat loss. We have previously demonstrated that isoflavones, such as genistein and daidzein, prevent muscle wasting in tumor-bearing mice. In this study, we examined the effect of morin, a flavonoid, on cachexia. The wet weight and myofiber size of muscles in Lewis lung carcinoma (LLC) cell-bearing mice fed a normal diet were decreased, compared with those in control mice fed a normal diet. In contrast, intake of morin prevented the reduction of muscle wet weight and myofiber size. Moreover, the tumor weight in mice fed the morin diet was lower than that in mice fed the normal diet. Both cell viability and protein synthetic ability of LLC cells were reduced by treatment with morin, but C2C12 myotubes were not affected. Binding assay using morin-conjugated magnetic beads identified ribosomal protein S10 (RPS10) as a target protein of morin. Consistent with the result of morin treatment, knockdown of RPS10 suppressed LLC cell viability. These results suggest that morin indirectly prevents muscle wasting induced by cancer cachexia by suppressing cancer growth via binding to RPS10. (出版サイトへのリンク) ● Publication site (DOI): 10.1016/j.bbrc.2018.10.184 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30389140 ● Summary page in Scopus @ Elsevier: 2-s2.0-85056802520 (DOI: 10.1016/j.bbrc.2018.10.184, PubMed: 30389140, Elsevier: Scopus)
15.	Chisato Tomida, Naoko Yakagishi, Hikaru Nagano, Takayuki Uchida, Ayako Maita, Katsuya Hirasaka, Takeshi Nikawa and Shigetada Kondo : VEGF pathway-targeting drugs induce evasive adaptation by activation of neuropilin-1/cMet in colon cancer cells., International Journal of Oncology, Vol.52, No.4, 1350-1362, 2018. (要約) Anti-angiogenic therapies targeting vascular endothelial growth factor (VEGF) and its receptor (VEGF-R) are important treatments for a number of human malignancies, including colorectal cancers. However, there is increasing evidence that VEGF/VEGF-R inhibitors promote the adaptive and evasive resistance of tumor cells to the therapies. The mechanism by which the cancer cells become resistant remains unclear. One potential mechanism is that VEGF/VEGF-R blockers directly act on tumor cells independently of anti-angiogenic effects. In this study, the direct effects of an anti-VEGF antibody (bevacizumab) and a VEGF-R tyrosine kinase inhibitor (sunitinib) on the evasive adaptation of colon cancer cells were compared. HCT116 and RKO human colon cancer cell lines were chronically exposed (3 months) to bevacizumab or sunitinib in vitro to establish bevacizumab- and sunitinib-adapted cells, respectively. Transwell migration and invasion assays, western blotting, reverse transcription-quantitative polymerase chain reaction, co-immunoprecipitation analysis, cell survival assays and ELISAs were conducted to analyze the adapted cells. Compared with the control vehicle-treated cells, the two cell models exhibited increased migration and invasion activities to different degrees and through different mechanisms. The bevacizumab-adapted cells, but not in the sunitinib-adapted cells, exhibited redundantly increased expression levels of VEGF/VEGF-R family members, including VEGF-A, placental growth factor, VEGF-C, VEGF-R1 and VEGF-R3. In addition, the phosphorylation levels of VEGF-R1 and VEGF-R3 were increased in the bevacizumab-adapted cells compared with the control cells. Thus, the inhibition of VEGF-R1 and VEGF-R3 decreased the evasive activities of the cells, suggesting that they remained dependent on redundant VEGF/VEGF-R signaling. By contrast, the sunitinib-adapted cells exhibited increased neuropilin-1 (NRP1) expression levels compared with the control cells. In the sunitinib-adapted cells, NRP1 interacted with phosphorylated cMet, and the cMet activation was dependent on NRP1. Thus, NRP1 or cMet blockade suppressed the evasive activation of the sunitinib-adapted cells. These results suggest that the sunitinib-adapted cells switched from a VEGF-R-dependent pathway to an alternative NRP1/cMet-dependent one. The findings of the present study indicate that VEGF/VEGF-R inhibitors directly act on colon cancer cells and activate their evasive adaptation via different mechanisms. (徳島大学機関リポジトリ) ● Metadata: 111606 (出版サイトへのリンク) ● Publication site (DOI): 10.3892/ijo.2018.4291 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29532881 ● Summary page in Scopus @ Elsevier: 2-s2.0-85042801496 (徳島大学機関リポジトリ: 111606, DOI: 10.3892/ijo.2018.4291, PubMed: 29532881, Elsevier: Scopus)
16.	Takayuki Uchida, Yoshihiro Sakashita, Kanako Kitahata, Yui Yamashita, Chisato Tomida, Yuki Kimori, Akio Komatsu, Katsuya Hirasaka, Ayako Maita, Reiko Nakao, Atsushi Higashitani, Akira Higashibata, Noriaki Ishioka, Toru Shimazu, Takeshi Kobayashi, Yuushi Okumura, Inho Choi, Motoko Oarada, M Edward Mills, Shigetada Kondo, Shin'ichi Takeda, Eiji Tanaka, Keiji Tanaka, Masahiro Sokabe and Takeshi Nikawa : Reactive oxygen species up-regulate expression of muscle atrophy-associated ubiquitin ligase Cbl-b in rat L6 skeletal muscle cells., American Journal of Physiology, Cell Physiology, Vol.314, No.6, C721-C731, 2018. (要約) Unloading-mediated muscle atrophy is associated with increased reactive oxygen species (ROS) production. We previously demonstrated that elevated ubiquitin ligase casitas B-lineage lymphoma-b (Cbl-b) resulted in the loss of muscle volume [Nakao R. et al. Mol Cell Biol, 29: 4798-4811, 2009]. However, the pathological role of ROS production associated with unloading-mediated muscle atrophy still remains unknown. Here, we showed the ROS-mediated signal transduction caused by microgravity or its simulation contributes to Cbl-b expression. In L6 myotubes, the assessment of redox status revealed that oxidized glutathione was increased under microgravity conditions, and simulated microgravity caused a burst of ROS, implicating ROS as a critical upstream mediator linking to downstream atrophic signaling. ROS generation activated the ERK1/2-early growth response protein (Egr) 1/2-Cbl-b signaling pathway, an established contributing pathway to muscle volume loss. Interestingly, antioxidant treatment, such as N-acetylcysteine and TEMPOL, but not catalase, blocked the clinorotation-mediated activation of ERK1/2. The increased ROS induced transcriptional activity of Egr 1 and/or Egr 2 to stimulate Cbl-b expression through the ERK 1/2 pathway in L6 myoblasts, since treatment with Egr 1/2 siRNA and an ERK 1/2 inhibitor significantly suppressed clinorotation-induced Cbl-b and Egr expression, respectively. Promoter and gel mobility shift assays revealed that Cbl-b was upregulated via an Egr consensus oxidative responsive element at -110 to -60 bp of the Cbl-b promoter. Together this indicates that under microgravity conditions, elevated ROS may be a crucial mechanotransducer in skeletal muscle cells, regulating muscle mass, through Cbl-b expression activated by the ERK-Egr signaling pathway. (徳島大学機関リポジトリ) ● Metadata: 111610 (出版サイトへのリンク) ● Publication site (DOI): 10.1152/ajpcell.00184.2017 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29513566 ● Search Scopus @ Elsevier (PMID): 29513566 ● Search Scopus @ Elsevier (DOI): 10.1152/ajpcell.00184.2017 (徳島大学機関リポジトリ: 111610, DOI: 10.1152/ajpcell.00184.2017, PubMed: 29513566)
17.	Manami Abe, Yuki Matsuo, Akiko Harada, Takayuki Uchida, Kanako Kitahata, Chisato Tomida, Katsuya Hirasaka, Shigetada Kondo, Nagakatsu Harada, Yutaka Nakaya, Hiroshi Sakaue, Reiko Nakao and Takeshi Nikawa : Distinct Gene Expression Profile Distinguishes Increased Metabolic Activity in Spontaneously Hyperactive Rats While Sedentary from That Induced by Exercise, Advances in Biological Chemistry, Vol.8, No.01, 1-14, 2018. (徳島大学機関リポジトリ) ● Metadata: 111609 (出版サイトへのリンク) ● Publication site (DOI): 10.4236/abc.2018.81001 (文献検索サイトへのリンク) ● Search Scopus @ Elsevier (DOI): 10.4236/abc.2018.81001 (徳島大学機関リポジトリ: 111609, DOI: 10.4236/abc.2018.81001)
18.	Chisato Tomida, Hikaru Nagano, Naoko Yamagishi, Takayuki Uchida, Ayako Maita, Katsuya Hirasaka, Takeshi Nikawa and Shigetada Kondo : Regorafenib induces adaptive resistance of colorectal cancer cells via inhibition of vascular endothelial growth factor receptor., The Journal of Medical Investigation : JMI, Vol.64, No.3-4, 262-265, 2017. (要約) Recently, inhibition of tumor angiogenesis has become an important anti-cancer therapy. Tumor angiogenesis is regulated by multiple signaling pathways, including VEGF and VEGF receptor (VEGF-R), FGF and FGF receptor (FGF-R), and PDGF and PDGF receptor (PDGF-R) pathways. Thus, the antiangiogenic agents, such as regorafenib, simultaneously target those receptors on vascular endothelial cells. In addition to endothelial cells, cancer cells express the three receptors, suggesting that the antiangiogenic inhibitors affect tumor cells. In fact, we previously demonstrated that regorafenib directly acted on human colorectal cancer cells and accelerated their apoptosis resistance and migration capability. Thus, we here elucidated how regorafenib induced the malignant phenotypes in colorectal cancer cells. To identify the responsible receptor among the regorafenib-targeting proangiogenic receptors, we examined the effects of a potent selective inhibitor for VEGF-R, FGF-R or PDGF-R on apoptosis resistance and migration capability. We clarified that blockade of VEGF-R, but not FGF-R and PDGF-R, induced the malignant phenotypes. We confirmed that blocking of VEGF ligands derived from colorectal cancer cells also induced the phenotypes. These results suggest that regorafenib progressed the malignancy via prevention of autocrine and paracrine VEGF signaling in colorectal cancer cells. J. Med. Invest. 64: 262-265, August, 2017. (キーワード) Angiogenesis Inhibitors / Apoptosis / Cell Movement / Colorectal Neoplasms / Drug Resistance, Neoplasm / HCT116 Cells / Humans / Phenylurea Compounds / Protein-Tyrosine Kinases / Pyridines / Receptors, Vascular Endothelial Growth Factor (徳島大学機関リポジトリ) ● Metadata: 111128 (出版サイトへのリンク) ● Publication site (DOI): 10.2152/jmi.64.262 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28954993 ● CiNii @ 国立情報学研究所 (CRID): 1390282679224220288 ● Summary page in Scopus @ Elsevier: 2-s2.0-85030250811 (徳島大学機関リポジトリ: 111128, DOI: 10.2152/jmi.64.262, PubMed: 28954993, CiNii: 1390282679224220288, Elsevier: Scopus)
19.	Chisato Tomida, Naoko Yamagishi, Hikaru Nagano, Takayuki Uchida, Ayako Maita, Katsuya Hirasaka, Takeshi Nikawa and Shigetada Kondo : Antiangiogenic agent sunitinib induces epithelial to mesenchymal transition and accelerates motility of colorectal cancer cells., The Journal of Medical Investigation : JMI, Vol.64, No.3-4, 250-254, 2017. (要約) Although vascular endothelial growth factor receptor (VEGF-R)-targeted antiangiogenic agents are important treatment for a number of human malignancies, there is accumulating evidence that the therapies may promote disease progression, such as invasion and metastasis. How tumors become to promote their evasiveness remains fully uncertain. One of possible mechanisms for the adaptation may be a direct effect of VEGF-R inhibitors on tumor cells expressing VEGF-R. To elucidate a direct effect of VEGF-R-targeting drug (sunitinib), we established a human colorectal cancer cell model adapted to sunitinib. The sunitinib-conditioned cells showed a significant increase in cellular motility and migration activities, compared to the vehicle-treated control cells. Consistent with the phenotype, the sunitinib-conditioned cells decreased the expression levels of E-cadherin (an epithelial marker), while significantly increased the levels of Slug and Zeb1 (mesenchymal markers). Expression profiles of VEGF-R in the sunitinib-conditioned cells showed that only neuropilin-1 (NRP1) expression was significantly increased among all VEGF-R tested. Blockade of NRP1 using its antagonist clearly repressed the migration activation in sunitinib-conditioned cells, but not in the control cells. These results suggest that inhibition of VEGF-R on colorectal cancer cells can drive the epithelial-mesenchymal transition, leading to activation of cell motility in an NRP1-dependent manner. J. Med. Invest. 64: 250-254, August, 2017. (キーワード) Angiogenesis Inhibitors / Cell Movement / Colorectal Neoplasms / Epithelial-Mesenchymal Transition / HCT116 Cells / Humans / Indoles / Neuropilin-1 / Pyrroles / Receptors, Vascular Endothelial Growth Factor / Transcriptome (徳島大学機関リポジトリ) ● Metadata: 111126 (出版サイトへのリンク) ● Publication site (DOI): 10.2152/jmi.64.250 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28954991 ● CiNii @ 国立情報学研究所 (CRID): 1390001204247522048 ● Summary page in Scopus @ Elsevier: 2-s2.0-85030217718 (徳島大学機関リポジトリ: 111126, DOI: 10.2152/jmi.64.250, PubMed: 28954991, CiNii: 1390001204247522048, Elsevier: Scopus)

総説・解説:

1.	内田貴之, 真板綾子, 二川健 : 微小重力環境を利用した筋萎縮機構の研究, 実験医学増刊号, Vol.38, No.7, 82-87, 2020年4月.
2.	内田貴之, 二川健, 中尾玲子 : 筋ミトコンドリアによる重力感知, 生体の科学, Vol.70, No.4, 301-305, 2019年5月. (キーワード) ミトコンドリア / 筋肉 / IGF-1 / メカノセンシング (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1521980704885620096 (CiNii: 1521980704885620096)
3.	内田貴之, 二川健 : 微小重力環境における筋萎縮発生メカニズムへの新展開, 月刊細胞, Vol.50, No.12, 618-621, 2018年10月.
4.	中尾玲子, 内田貴之, 二川健 : サルコペニアとメカニカルストレス, 診断と治療, Vol.106, No.6, 701-704, 2018年6月. (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1520573329924547328 (CiNii: 1520573329924547328)
5.	Yoshihiro Sakashita, 内田貴之, 二川健 : [Impacts of physical exercise on remodeling and hypertrophy of skeletal muscle.], Clinical Calcium, Vol.27, No.1, 79-85, 2017年. (要約) The skeletal muscle has high sensitivity for the mechanical stress. Because it is enlarged by training, whereas it is easily withered by lack of exercise. When we exercise, skeletal muscle cells per se sense mechanical loading, and muscular remodeling and the muscular hypertrophy occur. It has been revealed that the intracellular signaling through PGC-1 participates in the remodeling of the skeletal muscle, while PGC-14, an isoform of PGC-1, and the dystrophin-glycoprotein complex play important roles in muscular hypertrophy. This review describes the impact of physical exercise gives on the remodeling and hypertrophy of muscle through the signaling. (キーワード) Animals / Exercise / Humans / Hypertrophy / Insulin-Like Growth Factor I / Muscle, Skeletal / Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha / シグナル伝達 (signal transduction) (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28017949 ● Search Scopus @ Elsevier (PMID): 28017949 (PubMed: 28017949)
6.	Hikaru Kishimoto, 内田貴之, Kanako Kitahata, 二川健 : [Plasticity of skeletal muscle against unloading stress.], Clinical Calcium, Vol.27, No.3, 351-356, 2017年. (要約) Recently, muscle atrophy caused by unloading, such as spaceflight and bed rest has been becoming a social problem in Japan. However, the effective countermeasures against these disuse atrophy have not been developed. We have reviewed the mechanisms of disuse atrophy and its possible countermeasures. (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28232649 ● Search Scopus @ Elsevier (PMID): 28232649 (PubMed: 28232649)

国際会議:

1.	Takayuki Uchida, Miki Yukari, Katsuya Hirasaka, Sato Takahiko, Teranishi Mika, Ishihara Naotada, Kobayashi Takeshi, Higashitani Atsushi, Sokabe Masahiro and Takeshi Nikawa : The elucidation of mechanism by MFN2-mediated induction of disuse muscle atrophy, International Symposium on Mechanobiology for Human Health:8 years progress in The AMED-CREST/PRIME project on mechanobiplogy, Mar. 2023.
2.	Takeshi Nikawa, Takata Miho, Kosuke Sugiura, Takayuki Uchida, Iori Sakakibara, Madoka Uezumi and Akiyoshi Uezumi : Functional analysis of Aconitase2 in fetal skeletal muscle, International Symposium on Mechanobiology for Human Health:8 years progress in The AMED-CREST/PRIME project on mechanobiplogy, Mar. 2023.
3.	(名) Anaytulla, Takayuki Uchida, Miki Yukari, Sugiura Kohsuke, Ohno Ayako, Reiko Nakao and Takeshi Nikawa : Supplementation of Morin attenuates oxidative stress and muscle wasting in mouse C2C12 skeletal myotubes treated with dexamethasone, The 7th International Conference on Food Factors(ICoFF2019)/The 12th International Conference and Exhibition on Nutraceuticals and Functional Foods (ISNFF2019), Kobe, Dec. 2019.
4.	Takayuki Uchida, Sakashita Yoshihiro, Katsuya Hirasaka, Ohno Ayako, Reiko Nakao, Akira Higashibata, Kobayashi Takeshi, Sokabe Masahiro and Takeshi Nikawa : The influence of skeletal muscle thermogenesis on the regulation of body temperature during ketogenic diet-induced hypothermia, ADVANCED BIOMEDICAL ENGINEERING AND INSTRUMENTATION SUMMIT, San Francisco, Jun. 2019.
5.	Takeshi Nikawa, Takayuki Uchida, Ayako Maita and Reiko Nakao : Molecular mechanism and nutritional approach for unloading-mediated muscle atrophy, 2018 International Conference on Functional Food for improving Sarcopenia, Cachexia and Frailty, Mar. 2018.
6.	Takeshi Nikawa, Hashimoto Rie, Katsuya Hirasaka, Yano Chiaki, Aibara Kana, Takayuki Uchida, Tomoki Abe, Ayako Maita and Akama Kazuhito : Effects of dietary soy protein on unloading mediated muscle atrophy, 11th Asian Microgravity Symposium, Oct. 2016.
7.	Takayuki Uchida, Tomoki Abe, Ayako Maita, Reiko Nakao, Higashitani Atsushi, Kobayashi Takeshi, Sokabe Masahiro, Akira Higashibata and Takeshi Nikawa : Microgravity-induced signal transduction in skeletal muscle cells, 11th Asian Microgravity Symposium, Oct. 2016.

国内講演発表:

1.	伊藤千菜美, 鈴木穂, 松木大揮, ウラアナイツト, 内田貴之, 中森俊宏, 松井利郎, 二川健 : 大豆タンパク質の抗筋萎縮活性, 第56回日本栄養・食糧学会中国・四国支部大会, 2023年10月.
2.	津田晴香, 北畑香菜子, 内田貴之, 橋爪藤子, 東端晃, Junsoo Park, Inho Choi, 二川健 : 3D-clinorotation によるラットL6 筋管萎縮に対するC14-Cblin とセラストロールの同時投与による相加効果, 日本宇宙生物科学会第37回大会, 2023年9月.
3.	ANAYT ULLA, Mizanur Md Rahman, Takayuki Uchida, Hiroyuki Kayaki, Yosuke Nishitani, Susumu Yoshino, Hiroshige Kuwahara and Takeshi Nikawa : 3-(4-hydroxy-3-methoxyphenyl) propionic acid attenuates dexamethasone-induced muscle atrophy by suppressing Atrogin-1 and MuRF-1, 日本食品科学工学会第70回記念大会, Aug. 2023.
4.	伊藤千菜美, 松木大揮, 鈴木穂, 鴻野まどか, ウラアナイツト, 内田貴之, 石黒貴寛, 二川健 : 高野豆腐タンパク質の抗筋萎縮活性の解析, 第77回日本栄養・食糧学会大会, 2023年5月.
5.	内田貴之, 新垣翼, 津田晴香, 谷口瑠菜, 山本綾乃, 二川健 : 筋ミトコンドリアタンパク質Mitofusin2(Mfn2)による脂質代謝制御機構の解明, 第77回日本栄養・食糧学会大会, 2023年5月.
6.	津田晴香, 内田貴之, 川端いずみ, ウラアナイツト, 谷口瑠菜, 二川健 : 筋肉へのピセアタンノール作用の検討, 第77回日本栄養・食糧学会大会, 2023年5月.
7.	山野恵理華, 伊藤千菜美, 松木大揮, 鴻野まどか, ウラアナイツト, 内田貴之, 上番増喬, 高木均, 二川健 : セルロースナノファイバーの栄養学的機能性の検討, 第77回日本栄養・食糧学会大会, 2023年5月.
8.	津田晴香, 内田貴之, 川端いずみ, ANAYTULLA (名), 谷口瑠菜, 内田裕子, 森貞夫, 守田稔, 二川健 : C2C12 筋管細胞へのピセアタンノールの影響, 第55回日本栄養・食糧学会中国・四国支部大会, 2022年10月.
9.	谷口瑠菜, 北畑香菜子, 内田貴之, 加藤彩乃, 岸田昂大, 田中優佳子, Junsoo Park, Choi Inho, 二川健 : 3D-clinorotation によるラット L6 筋管萎縮に対する C14-Cblin とセラストロールの同時投与による相加効果, 第55回日本栄養・食糧学会中国・四国支部大会, 2022年10月.
10.	岸田昂大, 高田実穂, 杉浦宏祐, 内田貴之, 榊原伊織, 上住円, 上住聡芳, 二川健 : Aconitase2, 第55回日本栄養・食糧学会中国・四国支部大会, 2022年10月.
11.	高田実穂, 岸田昂大, 杉浦宏祐, 内田貴之, 榊原伊織, 上住円, 上住聡芳, 二川健 : 胎生期骨格筋における Aconitase2 の機能解析, 日本宇宙生物科学会第36回大会, 2022年9月.
12.	高田実穂, 榊原伊織, 岸田昂大, 福島拓, 新垣翼, 内田貴之, 布川朋也, 二川健 : 骨格筋におけるAconitase2の機能解明, 第76回日本栄養・食糧学会大会, 2022年6月.
13.	山崎穂, 松木大揮, 中野亘, 杉浦宏祐, 布川朋也, 内田貴之, 榊原伊織, 二川健 : 廃用性筋萎縮におけるアコニターゼ活性の低下とその栄養学的保護, 第76回日本栄養・食糧学会大会, 2022年6月.
14.	新垣翼, 谷口瑠菜, 青木栄理香, 佐藤文香, 高田実穂, 内田貴之, 二川健 : 高脂肪負荷食によるMfn2と骨格筋エネルギー代謝の関連解明, 第76回日本栄養・食糧学会大会, 2022年6月.
15.	中野亘, 杉浦宏祐, 内田貴之, 榊原伊織, 西良浩一, 二川健 : 廃用性萎縮筋におけるアコニターゼ活性とその保護, 第 54 回日本栄養•食糧学会中国•四国支部大会第7 回日本栄養改善学会四国支部学術総会合同大会, 2021年10月.
16.	足立雄一郎, 増田真志, 榊原伊織, 内田貴之, 大南博和, 奥村仙示, 二川健, 竹谷豊 : all trans レチノイン酸は小胞体ストレス応答関連因子 GADD34 の転写・転写後制御を介して筋繊維タイプ変化を引き起こす, 第 62 回日本生化学会中国・四国支部例会, 2021年9月.
17.	鴻野まどか, 内田貴之, 大石あかね, 平山楓子, 竹村祐馬, 髙尾正一郎, 金澤裕樹, 松元友暉, 原田雅史, 榊原伊織, 鈴木利雄, 二川健 : 蒸し大豆食品の継続摂取が運動不足の健常人の筋量や筋力に及ぼす影響, 第75回日本栄養・食糧学会大会, 2021年7月.
18.	谷口瑠菜, 川端いずみ, 内田貴之, ANAYTULLA (名), 榊原伊織, 二川健 : パッションフルーツ種子由来成分ピセアタンノールはデキサメタゾン誘導性筋萎縮を抑制する, 第75回日本栄養・食糧学会大会, 2021年7月.
19.	足立雄一郎, 増田真志, 榊原伊織, 内田貴之, 佐々木皓平, 野邊悠太郎, 大南博和, 大西康太, 奥村仙示, 山本浩範, 二川健, 竹谷豊 : all trans レチノイン酸は小胞体ストレス応答関連因子 GADD34 の発現制御を介して筋繊維タイプ変化を誘導する, 第 75 回日本栄養・食糧学会大会, 2021年7月.
20.	Iori Sakakibara, Kosuke Sugiura, Takayuki Uchida, Higashitani Atsushi, Kobayashi Takeshi, Sokabe Masahiro and Takeshi Nikawa : Mechano-signals regulate mitochondria-associated membrane, 第43回日本分子生物学会年会, Dec. 2020.
21.	加藤彩乃, 内田貴之, 榊原伊織, 池田泰隆, 濱田広一郎, 二川健 : 細胞内エネルギー代謝が筋細胞に与える影響, 第53回日本栄養食糧学会中国・四国支部大会, 2020年10月.
22.	中野亘, 三木裕可里, 杉浦宏祐, 榊原伊織, 内田貴之, 二川健 : ミトコンドリア小胞体接触領域 (MAM) を介した筋量調節メカニズムの解明, 第53回日本栄養食糧学会中国・四国支部大会, 2020年10月.
23.	杉浦宏祐, 内田貴之, 西良浩一, 二川健 : (ROS)Mitochondrial Aconitase, 35, 2020年10月.
24.	西良浩一, 杉浦宏祐, 内田貴之, 二川健 : ミトコンドリア-小胞体接触領域(MAM)は廃用性筋委縮を制御する(一般演題基礎:筋・腱・滑膜 ), 第93回日本整形外科学会学術総会【WEB】, 2020年5月.
25.	内田貴之, 三木裕加里, 杉浦宏祐, 真板綾子, 中尾玲子, 平坂勝也, 東谷篤志, 小林剛, 曽我部正博, 二川健 : 筋肉におけるミトコンドリアタンパク質Mfn2の役割, 第74回日本栄養・食糧学会大会, 2020年5月.
26.	藤岡大樹, 内田貴之, 杉浦宏祐, 小林剛, 東谷篤志, 曽我部正博, 二川健 : Unloadingによる筋萎縮におけるCa2+-ROSシグナルの変化, 第74回日本栄養・食糧学会大会, 2020年5月.
27.	加藤彩乃, 内田貴之, 杉浦宏祐, 池田泰隆, 濱田広一郎, 二川健 : 細胞内エネルギー代謝経路が筋繊維タイプに与える影響, 第74回日本栄養・食糧学会大会, 2020年5月.
28.	川端いずみ, 内田貴之, 加藤彩乃, Anaytulla (名), 内田裕子, 森貞夫, 森田稔, 二川健 : ピセアタンノールの筋萎縮抑制効果の検討, 第74回日本栄養・食糧学会大会, 2020年5月.
29.	新井田裕樹, 増田真志, 吉澤和香, 足立雄一郎, 大西康太, 大南博和, 内田貴之, 奥村仙示, 二川健, 山本浩範, 竹谷豊 : 慢性腎臓病による骨格筋の脂肪酸代謝異常を介した脂肪毒性(Liptoxicity)は筋委縮(サルコペニア) を惹起する, 第23回日本病態栄養学会年次集会, 2020年1月.
30.	平坂勝也, M.Mills Edward, 内田貴之, Ohno Ayako, 二川健 : New aspect of mitochondrial uncoupling protein(UCP):Identification of UCP3 interacting proteins, 第42回日本分子生物学会年会, 2019年12月.
31.	川端いずみ, 内田貴之, 加藤彩乃, Anaytulla (名), 内田裕子, 森貞夫, 森田稔, 二川健 : ピセアタンノールの筋萎縮抑制効果の検討, 第52回日本栄養・食慮学会中国・四国支部大会, 2019年10月.
32.	新井田裕樹, 増田真志, 吉澤和香, 足立雄一郎, 大西康太, 大南博和, 内田貴之, 奥村仙示, 二川健, 山本浩範, 竹谷豊 : 慢性腎臓病モデルラットの骨格筋における脂肪酸代謝異常が及ぼす筋萎縮への影響, 第66回日本栄養改善学会学術集会, 2019年9月.
33.	杉浦宏祐, 内田貴之, 真板綾子, 中尾玲子, 平坂勝也, 東谷篤志, 東端晃, 小林剛, 曽我部正博, 西良浩一, 二川健 : 廃用性筋萎縮におけるミトコンドリア形態変化及び酸化ストレス発生による影響, 日本筋学会第5回学術集会, 2019年8月.
34.	足立雄一郎, 増田真志, 新井田裕樹, 大西康太, 内田貴之, 奥村仙示, 山本浩範, 二川健, 竹谷豊 : レチノイン酸による小胞体ストレス感受性の影響, 日本ビタミン学会第71回大会, 2019年6月.
35.	三木裕加里, 小松明生, 内田貴之, 中尾玲子, 真板綾子, 曽我部正博, 二川健 : 廃用性筋萎縮進展におけるミトコンドリアタンパク質Mfn2の役割, 第73回日本栄養・食糧学会大会, 2019年5月.
36.	内田貴之, 三木裕加里, 坂下禎宏, 真板綾子, 中尾玲子, 平坂勝也, 東谷篤志, 東端晃, 小林剛, 曽我部正博, 二川健 : ミトコンドリアを介した無重力ストレス感知機構の解明, 第73回日本栄養・食糧学会大会, 2019年5月.
37.	内田貴之, 真板綾子, 中尾玲子, 二川健 : 宇宙医学から健康長寿へ, 第221回徳島医学会学術集会, 2019年2月. (キーワード) 筋萎縮 (muscle atrophy) / ミトコンドリア (mitochondria)
38.	二川健, 内田貴之, 中尾玲子, 平坂勝也, 真板宣夫, 東谷篤志, 小林剛, 石原直忠, 曽我部正博 : Unloadingストレスに対する筋細胞の初期応答:酸化ストレスの重要性, 第41回日本分子生物学会年会, 2018年11月.
39.	足立雄一郎, 増田真志, 新井田裕樹, 大西康太, 内田貴之, 奥村仙示, 二川健, 竹谷豊 : 小胞体ストレス誘導下におけるレチノイン酸の影響, 第51回日本栄養・食糧学会中国・四国支部大会, 2018年11月.
40.	三木裕加里, 内田貴之, 木森有希, 坂下禎宏, 小松明生, 真板綾子, 中尾玲子, 内田実佑, 藤岡大樹, 小林剛, 東谷篤志, 石原直忠, 東端晃, 石岡憲昭, 武田伸一, 曽我部正博, 二川健 : ユビキチンリガーゼCbl-bは無重力ストレス誘導性の酸化ストレスにより増大する, 第51回日本栄養・食糧学会中国・四国支部大会, 2018年11月.
41.	三木裕加里, 内田貴之, 木森有希, 坂下禎宏, 小松明生, 真板綾子, 中尾玲子, 内田実佑, 藤岡大樹, 小林剛, 東谷篤志, 石原直忠, 東端晃, 石岡憲昭, 武田伸一, 曽我部正博, 二川健 : 酸化ストレスはラットL6細胞におけるユビキチンリガーゼCbl-bの発現を増大する, 日本宇宙生物科学会第32回大会, 2018年9月.
42.	小松明生, 内田貴之, 北畑香菜子, 真板綾子, 中尾玲子, 瀬川圭, 二川健 : 廃用性筋萎縮を抑制するユビキチンリガーゼCbl-bの低分子阻害剤の開発, 日本筋学会第4回学術集会, 2018年8月.
43.	真板綾子, 真板宣夫, 奥村裕司, 内田貴之, 中尾玲子, 岸本幸治, 二川健 : 高病原性インフルエンザ感染に関わる宿主酵素MSPLと阻害剤との複合体構造., 病態プロテアーゼ学会, 2018年8月.
44.	新井田裕樹, 増田真志, 吉澤和香, 足立雄一郎, 内田貴之, 大西康太, 河合慶親, 二川健, 山本浩範, 竹谷豊 : 慢性腎臓病に伴う骨格筋の飽和脂肪酸蓄積はオートファジー不全を介して筋萎縮を誘発する, 日本ビタミン学会第70回大会(高槻現代劇場), 2018年6月.
45.	二宮みゆき, 木森有希, 小松明生, 鉄野文香, 三木裕加里, 北畑香菜子, 内田貴之, 真板綾子, 中尾玲子, 松井利郎, 赤間一仁, 二川健 : 廃用性筋萎縮を防ぐ高機能米の開発, 第72回日本栄養・食糧学会大会, 2018年5月.
46.	吉田里沙, 新井田裕樹, 足立雄一郎, 酒井晶子, 奥村仙示, 大西康太, 内田貴之, 河合慶親, 山本浩範, 二川健, 竹谷豊, 増田真志 : スルフォラファンのリポファジーを介した脂肪分解効果, 第72回日本栄養・食糧学会大会(岡山県立大学), 2018年5月.
47.	木森有希, 二宮みゆき, 三木裕加里, 小松明生, 鉄野文香, 内田貴之, 中尾玲子, 真板綾子, 近藤茂忠, 曽我部正博, 二川健 : 無重力環境におけるミトコンドリアタンパク質Mitofusin2(Mfn2)の役割, 第72回日本栄養・食糧学会大会, 2018年5月.
48.	内田貴之, 木森有希, 坂下禎宏, 真板綾子, 中尾玲子, 平坂勝也, 東谷篤志, 東端晃, 小林剛, 曽我部正博, 武田伸一, 二川健 : 無重力による廃用性筋萎縮における酸化ストレスの重要性, 第72回日本栄養・食糧学会大会, 2018年5月.
49.	内田貴之 : 無重力による酸化ストレスを介した筋細胞内シグナルトランスダクション, Genes to Cells, 2017年12月.
50.	三木裕加里, 内田貴之, 木森有希, 坂下宏, 真板綾子, 中尾玲子, 小林剛, 東谷篤志, 石原直忠, 武田伸一, 曽我部正博, 二川健 : 無重力ストレスによる筋萎縮における酸化ストレスの重要性, 第50回日本栄養・食糧学会中国・四国支部大会, 2017年11月.
51.	内田貴之 : 無重力による酸化ストレスを介した筋細胞のシグナルトランスダクション, 宇宙生物科学, 2017年9月.
52.	内田貴之 : 無重力ストレスによる筋萎縮における酸化ストレスの重要性, 第3回Neo VitamineD Workshop 学術集会, 2017年8月.
53.	内田貴之, 真板綾子, 中尾玲子, 小林剛, 東谷篤志, 石原直忠, 武田伸一, 曽我部正博, 二川健 : 無重力ストレスによる筋萎縮における酸化ストレスの重要性, 日本筋学会第3回学術集会, 2017年8月.
54.	二宮みゆき, 木森有希, 髙木麻理奈, 井田くるみ, 岸本ひかる, 高津絵梨香, 石田祐子, 加藤健, 越智ありさ, 内田貴之, 真板綾子, 安倍知紀, 近藤茂忠, 中尾玲子, 平坂勝也, 二川健 : 坐骨神経切除による筋萎縮におけるホエイペプチドと大豆タンパク質の阻害効果, 第71回日本栄養・食糧学会大会, 2017年5月.
55.	内田貴之, 木森有希, 二宮みゆき, 坂下宏, 安倍知紀, 真板綾子, 中尾玲子, 平坂勝也, 東谷篤志, 小林剛, 曽我部正博, 武田伸一, 二川健 : 無重力による酸化ストレス産生を介した筋細胞内シグナル・トランスダクション, 第71回日本栄養・食糧学会大会, 2017年5月.
56.	木森有希, 二宮みゆき, 相原知佳, 坂下宏, 内田貴之, 安倍知紀, 中尾玲子, 真板綾子, 近藤茂忠, 二川健 : Mfn2ノックダウンの筋肉における影響の検討, 第71回日本栄養・食糧学会大会, 2017年5月.
57.	二宮みゆき, 髙木麻理奈, 井田くるみ, 岸本ひかる, 高津絵梨香, 石田祐子, 加藤健, 越智ありさ, 内田貴之, 真板綾子, 安倍知紀, 近藤茂忠, 中尾玲子, 平坂勝也, 二川健 : 坐骨神経切除による筋萎縮に対するホエイペプチドと大豆タンパク質の効果, 第49回日本栄養・食糧学会中国・四国支部大会, 2016年11月.

その他・研究会:

1.	二川健, 内田貴之, 真板綾子, 中尾玲子, 平坂勝也, 小林剛, 曽我部正博, 東谷篤志, 武田伸一 : 廃用性筋萎縮における酸化ストレスの重要性, 国立研究開発法人国立精神・神経医療研究センター精神・神経疾患研究開発費「ジストロフィン欠損モデル動物を基盤とした筋ジストロフィーの新しい治療法開発」平成30年度班会議, 2018年12月.
2.	二川健, 内田貴之, 真板綾子, 中尾玲子, 小林剛, 曽我部正博, 武田伸一 : 無重力(Unloading)ストレスによる筋細胞のシグナルトランスダクション, 国立研究開発法人国立精神・神経医療研究センター精神・神経疾患研究開発費「ジストロフィン欠損モデル動物を基盤とした筋ジストロフィーの新しい治療法開発」平成29年度班会議, 2017年12月.
3.	二川健, 内田貴之, 真板綾子, 中尾玲子 : 無重力環境で培養した筋細胞のメタボローム解析, 第2回メタボローム解析シンポジウム, 2017年6月.

科学研究費補助金 (KAKEN Grants Database @ NII.ac.jp)

廃用性筋萎縮に繋がるミトコンドリア-小胞体連関による新規鉄代謝制御システムの解明 (研究課題/領域番号: 23K10846 )
ストレス応答分子HO-1を介した新規抗筋萎縮シグナルの解明 (研究課題/領域番号: 20K19639 )
長期間の重力変化に対するマウス骨格筋の適応メカニズム追究 (研究課題/領域番号: 19KK0253 )
筋萎縮に対する新規栄養学的アプローチ：鉄代謝とエネルギー産生系をつなぐ観点から (研究課題/領域番号: 18K17968 )
研究者番号（00803561）による検索

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講師 : 内田貴之