徳島大学 / 教育研究者総覧 --- 中尾玲子

専門分野

研究テーマ

著書・論文

学術論文(審査論文):

1.	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)
2.	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)
3.	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)
4.	Kazuhito Akama, Yasuka Shimajiri, Kumiko Kainou, Ryota Iwasaki, Reiko Nakao, Takeshi Nikawa and Akio Nishikawa : Functional rice with tandemly repeated Cbl-b ubiquitin ligase inhibitory pentapeptide prevents denervation-induced muscle atrophy in vivo, Bioscience, Biotechnology, and Biochemistry, Vol.85, No.6, 1415-1421, 2021. (要約) Ubiquitin ligase Casitas B-lineage lymphoma-b (Cbl-b) play a critical role in nonloading-mediated skeletal muscle atrophy: Cbl-b ubiquitinates insulin receptor substrate-1 (IRS-1), leading to its degradation and a resulting loss in muscle mass. We reported that intramuscular injection of a pentapeptide, DGpYMP, which acts as a mimic of the phosphorylation site in IRS-1, significantly inhibited denervation-induced skeletal muscle loss. In order to explore the possibility of the prevention of muscle atrophy by diet therapy, we examined the effects of oral administration of transgenic rice containing Cblin (Cbl-b inhibitor) peptide (DGYMP) on denervation-induced muscle mass loss in frogs. We generated transgenic rice seeds in which 15 repeats of Cblin peptides with a WQ spacer were inserted into the rice storage protein glutelin. A diet of the transgenic rice seeds had significant inhibitory effects on denervation-induced atrophy of the leg skeletal muscles in frogs, compared with those receiving a diet of wild-type rice. (キーワード) Animals / Denervation / Enzyme Inhibitors / Mice / Muscular Atrophy / Oryza / Plants, Genetically Modified / Proto-Oncogene Proteins c-cbl / Tandem Repeat Sequences (出版サイトへのリンク) ● Publication site (DOI): 10.1093/bbb/zbab059 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33864463 ● Summary page in Scopus @ Elsevier: 2-s2.0-85107090566 (DOI: 10.1093/bbb/zbab059, PubMed: 33864463, Elsevier: Scopus)
5.	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)
6.	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)
7.	Reiko Nakao, Tomoki Abe, Saori Yamamoto and Katsutaka Oishi : Ketogenic diet induces skeletal muscle atrophy via reducing muscle protein synthesis and possibly activating proteolysis in mice., Scientific Reports, Vol.9, No.1, 2019. (徳島大学機関リポジトリ) ● Metadata: 115566 (出版サイトへのリンク) ● Publication site (DOI): 10.1038/s41598-019-56166-8 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31873138 ● Search Scopus @ Elsevier (PMID): 31873138 ● Search Scopus @ Elsevier (DOI): 10.1038/s41598-019-56166-8 (徳島大学機関リポジトリ: 115566, DOI: 10.1038/s41598-019-56166-8, PubMed: 31873138)
8.	Ryo Katsuki, Shinji Sakata, Reiko Nakao, Katsutaka Oishi and Yasunori Nakamura : Lactobacillus curvatus CP2998 Prevents Dexamethasone-Induced Muscle Atrophy in C2C12 Myotubes., Journal of Nutritional Science and Vitaminology, Vol.65, No.5, 455-458, 2019. (キーワード) Animals / Bacterial Proteins / Cell Culture Techniques / Dexamethasone / Dose-Response Relationship, Drug / Fermented Foods and Beverages / Glucocorticoids / Lactobacillus / Mice / Muscle Fibers, Skeletal / Muscle Proteins / Muscular Atrophy / RNA, Messenger / SKP Cullin F-Box Protein Ligases / Tripartite Motif Proteins / Ubiquitin-Protein Ligases (出版サイトへのリンク) ● Publication site (DOI): 10.3177/jnsv.65.455 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31666484 ● Search Scopus @ Elsevier (PMID): 31666484 ● Search Scopus @ Elsevier (DOI): 10.3177/jnsv.65.455 (DOI: 10.3177/jnsv.65.455, PubMed: 31666484)
9.	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)
10.	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)
11.	Reiko Nakao, Shigeki Shimba and Katsutaka Oishi : Ketogenic diet induces expression of the muscle circadian gene Slc25a25 via neural pathway that might be involved in muscle thermogenesis., Scientific Reports, Vol.7, No.1, 2885, 2017. (要約) -sensitive ATP carrier in the inner mitochondrial membrane, fluctuates in a circadian manner in mouse skeletal muscle. We showed here that the circadian expression of muscle Slc25a25 was damped in Clock mutant, muscle-specific Bmal1-deficient, and global Bmal1-deficient mice. Furthermore, a ketogenic diet (KD) that induces time-of-day-dependent hypothermia (torpor), induced Slc25a25 mRNA expression in skeletal muscle. Hypothermia induced by KD did not affect thermogenic genes such as Sarcolipin and Pgc1a in muscles and Ucp1 in adipose tissues. Sciatic denervation abolished circadian and KD-induced Slc25a25 expression, suggesting that the circadian clock regulates muscle Slc25a25 expression via neural pathways. We measured body temperature (Tb) in sciatic denervated mice fed with KD to determine the functional role of KD-induced Slc25a25 expression. Sciatic denervation abolished Slc25a25 expression and augmented KD-induced hypothermia compared with sham-operated mice, but did not affect Tb in mice given a normal diet. These findings suggest that KD feeding induces expression of the muscle circadian gene Slc25a25 via neural pathways, and that SLC25A25 might be involved in muscle thermogenesis under KD-induced hypothermia in mammals. (徳島大学機関リポジトリ) ● Metadata: 112407 (出版サイトへのリンク) ● Publication site (DOI): 10.1038/s41598-017-03119-8 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28588221 ● Search Scopus @ Elsevier (PMID): 28588221 ● Search Scopus @ Elsevier (DOI): 10.1038/s41598-017-03119-8 (徳島大学機関リポジトリ: 112407, DOI: 10.1038/s41598-017-03119-8, PubMed: 28588221)
12.	Reiko Nakao, Hiroki Okauchi, Chiaki Hashimoto, Naoyuki Wada and Katsutaka Oishi : Determination of reference genes that are independent of feeding rhythms for circadian studies of mouse metabolic tissues., Molecular Genetics and Metabolism, Vol.121, No.2, 190-197, 2017. (要約) Real-time reverse transcription-polymerase chain reaction (RT-PCR) analysis is a popular method for the measurement of mRNA expression level and is a critical tool for basic research. The identification of suitable reference genes that are stable and not affected by experimental conditions is a critical step in the accurate normalization of RT-PCR. On the other hand, the levels of numerous transcripts exhibit circadian oscillation in various peripheral tissues and it is thought to be regulated by feeding rhythms in addition to the molecular circadian clock. Here, we investigated the effects of feeding schedule on the temporal expression profiles of 13 common housekeeping genes in metabolic tissues of mice fed during either the sleep or the active phase. The expression of most of these genes fluctuated dependently on feeding rhythms in the liver and WAT, but not in skeletal muscle. Two-way analyses of variance (ANOVA) identified 18S ribosomal RNA (Rn18s) as the only gene that was stably expressed throughout the day independently of feeding schedules in the liver and WAT, although RefFinder software showed that peptidylprolyl isomerase A (Ppia) was the most stably expressed housekeeping gene. Both ANOVA and RefFinder software determined that Actb was the preferred reference gene for skeletal muscle. Furthermore, NormFinder proposed that the optimal pairs of reference genes were beta-2 microglobulin (B2m)-Ppia in the liver, Ppia-TATA box binding protein (Tbp) in WAT, and tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein, zeta polypeptide (Ywhaz)-glyceraldehyde-3-phosphate dehydrogenase (Gapdh) in skeletal muscle, and that their stability value was better than that of a single stable gene. The appropriate reference gene pairs for normalizing genes of interest in mouse circadian studies are B2m-Ppia in the liver, Ppia-Tbp in WAT, and Ywhaz-Gapdh in skeletal muscle. (出版サイトへのリンク) ● Publication site (DOI): 10.1016/j.ymgme.2017.04.001 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28410879 ● Search Scopus @ Elsevier (PMID): 28410879 ● Search Scopus @ Elsevier (DOI): 10.1016/j.ymgme.2017.04.001 (DOI: 10.1016/j.ymgme.2017.04.001, PubMed: 28410879)

総説・解説:

1.	中尾玲子 : ケトジェニックダイエット摂取に対する骨格筋の応答, 生化学, Vol.94, No.5, 730-734, 2022年10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.	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)
4.	Reiko Nakao, Takeshi Nikawa and Katsutaka Oishi : The skeletal muscle circadian clock: current insights, ChronoPhysiology and Therapy, Vol.7, 47-57, Nov. 2017. (出版サイトへのリンク) ● Publication site (DOI): 10.2147/CPT.S116569 (文献検索サイトへのリンク) ● Search Scopus @ Elsevier (DOI): 10.2147/CPT.S116569 (DOI: 10.2147/CPT.S116569)

国際会議:

1.	(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.
2.	Reiko Nakao and Takeshi Nikawa : The influence of skeletal muscle thermogenesis on the regulation of body temperature during ketogenic diet-induced hypothermia, European Biological Rhythms Society 2019, Aug. 2019.
3.	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.
4.	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.
5.	Reiko Nakao, Shigeki Shimba and Katsutaka Oishi : Chronic starvation induce expression of the muscle circadian gene SLC25A25 via neural pathway that might be involved in muscle, XV European Biological Rhythms Society Congress, Jul. 2017.
6.	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.	Reiko Nakao, Takeshi Nikawa and Katsutaka Oishi : Skeletal muscle thermogenesis during ketogenic diet-induced hypothermia, 第43回日本分子生物学会年会, Dec. 2020.
2.	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.
3.	佐藤友紀, 中尾玲子, 山本彩音, 二川健 : 大豆タンパク質の摂取はケトジェニックダイエットによる体温の日内リズム乱れを改善する, 第74回日本栄養・食糧学会大会, 2020年5月.
4.	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.
5.	中尾玲子, 安倍知紀, 山本幸織, 大石勝隆 : ケトジェニックダイエットはユビキチン・プロテアソーム系及びオートファジー系を活性化し，マウス骨格筋を萎縮させる, 第73回日本栄養・食糧学会大会, 2019年5月.
6.	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.
7.	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.
8.	中尾玲子, 宮脇克行, 出口祥啓, 髙橋章, 二川健 : 宇宙栄養・食糧関連技術の開発とGatewayへの期待, 国際宇宙探査ワークショップ(その2), 2019年3月.
9.	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)
10.	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.
11.	佐藤友紀, 中尾玲子, 赤間一仁, 二川健 : Cbl-b阻害ペプチド高含有米の除神経性筋萎縮改善作用の評価, 第51回日本栄養・食糧学会中国・四国支部大会, 2018年11月.
12.	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.
13.	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.
14.	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.
15.	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.
16.	中尾玲子, 山本(肥後) 明花, 尾﨑順子, 大和田一雄, 大石勝隆 : シリアンハムスターとマウスにおける除神経性筋萎縮の比較, 第2回冬眠休眠研究会, 2018年6月.
17.	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.
18.	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.
19.	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.
20.	中尾玲子, 榛葉繁紀, 大石勝隆 : 低栄養状態での体温維持における骨格筋の寄与-日周発現遺伝子Slc25a25の役割-, 第13回環境生理学プレコングレス, 2018年3月.
21.	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.
22.	中尾玲子, 榛葉繁紀, 大石勝隆 : 骨格筋特異的な熱産生遺伝子Slc25a25は飢餓時の熱産生を制御する, 第18回運動器科学研究会, 2017年9月.
23.	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.
24.	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.
25.	中尾玲子, 岡内宏樹, 橋本千秋, 大石勝隆 : 末梢組織におけるハウスキーピング遺伝子の日周変動と食餌リズムの影響, 第71回日本栄養・食糧学会大会, 2017年5月.
26.	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.
27.	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.
28.	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)

クマの冬眠における体内時計を介した代謝抑制機構の解明 (研究課題/領域番号: 20KK0355 )
老人性低体温症モデルマウスを用いた骨格筋の新規熱産生メカニズムの解明 (研究課題/領域番号: 18K10994 )
冬眠動物における骨格筋萎縮耐性メカニズムの解明とサルコペニア対策への応用 (研究課題/領域番号: 15K16499 )
廃用性筋萎縮の新たなメカニズムの解明：体内時計の乱れは筋肉をも壊してしまうのか？ (研究課題/領域番号: 24620015 )
研究者番号（20582696）による検索

講師 : 中尾玲子

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講師 : 中尾 玲子

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

講師 : 中尾玲子