Tokushima University / Educator and Researcher Directory --- Nakao, Reiko

Field of Study

Subject of Study

Book / Paper

Academic Paper (Judged Full Paper):

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. (Summary) 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. (Keyword) 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 (Link to Publication Site) ● Publication site (DOI): 10.1093/bbb/zbac140 (Link to Search Site for Scientific Articles) ● 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. (Summary) 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. (Tokushima University Institutional Repository) ● Metadata: 117588 (Link to Publication Site) ● Publication site (DOI): 10.1038/s41538-021-00108-0 (Link to Search Site for Scientific Articles) ● 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 (Tokushima University Institutional Repository: 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. (Tokushima University Institutional Repository) ● Metadata: 116581 (Link to Publication Site) ● Publication site (DOI): 10.1002/jor.25131 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34185335 ● Summary page in Scopus @ Elsevier: 2-s2.0-85109422486 (Tokushima University Institutional Repository: 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. (Summary) 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. (Keyword) Animals / Denervation / Enzyme Inhibitors / Mice / Muscular Atrophy / Oryza / Plants, Genetically Modified / Proto-Oncogene Proteins c-cbl / Tandem Repeat Sequences (Link to Publication Site) ● Publication site (DOI): 10.1093/bbb/zbab059 (Link to Search Site for Scientific Articles) ● 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. (Summary) 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. (Keyword) Animals / Cell Line / Dexamethasone / Dose-Response Relationship, Drug / Flavonoids / Mice / Muscle Fibers, Skeletal / Muscle Proteins / Muscular Atrophy / Oxidative Stress (Tokushima University Institutional Repository) ● Metadata: 116344 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.abb.2021.108873 (Link to Search Site for Scientific Articles) ● 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 (Tokushima University Institutional Repository: 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. (Summary) 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. (Keyword) Animals / Birds / Crystallography, X-Ray / Humans / Influenza in Birds / Membrane Proteins / Orthomyxoviridae / Protein Conformation / Serine Endopeptidases (Tokushima University Institutional Repository) ● Metadata: 116821 (Link to Publication Site) ● Publication site (DOI): 10.26508/LSA.202000849 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33820827 ● Summary page in Scopus @ Elsevier: 2-s2.0-85103997820 (Tokushima University Institutional Repository: 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. (Tokushima University Institutional Repository) ● Metadata: 115566 (Link to Publication Site) ● Publication site (DOI): 10.1038/s41598-019-56166-8 (Link to Search Site for Scientific Articles) ● 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 (Tokushima University Institutional Repository: 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. (Keyword) 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 (Link to Publication Site) ● Publication site (DOI): 10.3177/jnsv.65.455 (Link to Search Site for Scientific Articles) ● 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. (Summary) 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. (Tokushima University Institutional Repository) ● Metadata: 111610 (Link to Publication Site) ● Publication site (DOI): 10.1152/ajpcell.00184.2017 (Link to Search Site for Scientific Articles) ● 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 (Tokushima University Institutional Repository: 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. (Tokushima University Institutional Repository) ● Metadata: 111609 (Link to Publication Site) ● Publication site (DOI): 10.4236/abc.2018.81001 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.4236/abc.2018.81001 (Tokushima University Institutional Repository: 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. (Summary) -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. (Tokushima University Institutional Repository) ● Metadata: 112407 (Link to Publication Site) ● Publication site (DOI): 10.1038/s41598-017-03119-8 (Link to Search Site for Scientific Articles) ● 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 (Tokushima University Institutional Repository: 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. (Summary) 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. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.ymgme.2017.04.001 (Link to Search Site for Scientific Articles) ● 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)

Review, Commentary:

1.	Reiko Nakao : Response of skeletal muscle under ketogenic diet, Seikagaku, Vol.94, No.5, 730-734, Oct. 2022. (Link to Publication Site) ● Publication site (DOI): 10.14952/seikagaku.2022.940730 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390293887769000960 ● Search Scopus @ Elsevier (DOI): 10.14952/seikagaku.2022.940730 (DOI: 10.14952/seikagaku.2022.940730, CiNii: 1390293887769000960)
2.	Takayuki Uchida, Takeshi Nikawa and Reiko Nakao : Mitochondria-mediated mechanosensing mechanism in skeletal muscle, Science of the Living Body, Vol.70, No.4, 301-305, May 2019. (Keyword) ミトコンドリア / 筋肉 / IGF-1 / メカノセンシング (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1521980704885620096 (CiNii: 1521980704885620096)
3.	Reiko Nakao, Takayuki Uchida and Takeshi Nikawa : 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, Jun. 2018. (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (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. (Link to Publication Site) ● Publication site (DOI): 10.2147/CPT.S116569 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.2147/CPT.S116569 (DOI: 10.2147/CPT.S116569)

Proceeding of International Conference:

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.

Proceeding of Domestic Conference:

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.	Takayuki Uchida, Yukari Miki, Kosuke Sugiura, Ayako Maita, Reiko Nakao, 平坂勝也, 東谷篤志, 小林剛, 曽我部正博 and Takeshi Nikawa : 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, May 2020.
3.	佐藤友紀, Reiko Nakao, 山本彩音 and Takeshi Nikawa : 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, May 2020.
4.	Kohsuke Sugiura, Takayuki Uchida, Ayako Maita, Reiko Nakao, Katsuya Hirasaka, 東谷篤志, Akira Higashibata, 小林剛, 曽我部正博, Koichi Sairyo and Takeshi Nikawa : 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, Aug. 2019.
5.	Reiko Nakao, 安倍知紀, 山本幸織 and 大石勝隆 : Ketogenic diet induces skeletal muscle atrophy via activation of ubiquitin proteasome and autophagy-lysosome pathways in mice, 第73回日本栄養・食糧学会大会, May 2019.
6.	Yukari Miki, Akio Komatsu, Takayuki Uchida, Reiko Nakao, Ayako Maita, 曽我部正博 and Takeshi Nikawa : 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, May 2019.
7.	Takayuki Uchida, Yukari Miki, Yoshihiro Sakashita, 真板綾子, Reiko Nakao, Katsuya Hirasaka, 東谷篤志, Akira Higashibata, 小林剛, 曽我部正博 and Takeshi Nikawa : 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, May 2019.
8.	Reiko Nakao, Katsuyuki Miyawaki, Yoshihiro Deguchi, Akira Takahashi and Takeshi Nikawa : 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), Mar. 2019.
9.	Takayuki Uchida, Ayako Maita, Reiko Nakao and Takeshi Nikawa : 宇宙医学から健康長寿へ, 第221回徳島医学会学術集会, Feb. 2019. (Keyword) muscle atrophy / mitochondria
10.	Takeshi Nikawa, Takayuki Uchida, Reiko Nakao, Katsuya Hirasaka, Nobuo Maita, 東谷篤志, 小林剛, 石原直忠 and 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, Nov. 2018.
11.	Yuki Satoh, Reiko Nakao, 赤間一仁 and Takeshi Nikawa : 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, Nov. 2018.
12.	Yukari Miki, Takayuki Uchida, Yuki Kimori, Yoshihiro Sakashita, Akio Komatsu, Ayako Maita, Reiko Nakao, Miyu Uchida, Taiju Fujioka, 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 and Takeshi Nikawa : 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, Nov. 2018.
13.	Yukari Miki, Takayuki Uchida, Yuki Kimori, Yoshihiro Sakashita, Akio Komatsu, Ayako Maita, Reiko Nakao, Miyu Uchida, Taiju Fujioka, 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 and Takeshi Nikawa : 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, Sep. 2018.
14.	Akio Komatsu, Takayuki Uchida, Kanako Kitahata, Ayako Maita, Reiko Nakao, 瀬川圭 and Takeshi Nikawa : 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, Aug. 2018.
15.	Ayako Maita, Nobuo Maita, Yuushi Okumura, Takayuki Uchida, Reiko Nakao, Koji Kishimoto and Takeshi Nikawa : 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, Aug. 2018.
16.	Reiko Nakao, 山本(肥後) 明花, 尾﨑順子, 大和田一雄 and 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, Jun. 2018.
17.	Miyuki Ninomiya, Yuki Kimori, Akio Komatsu, Ayaka Tetsuno, Yukari Miki, Kanako Kitahata, Takayuki Uchida, Ayako Maita, Reiko Nakao, 松井利郎, 赤間一仁 and Takeshi Nikawa : 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, May 2018.
18.	Yuki Kimori, Miyuki Ninomiya, Yukari Miki, Akio Komatsu, Ayaka Tetsuno, Takayuki Uchida, Reiko Nakao, Ayako Maita, 近藤茂忠, 曽我部正博 and Takeshi Nikawa : 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, May 2018.
19.	Takayuki Uchida, Yuki Kimori, Yoshihiro Sakashita, Ayako Maita, Reiko Nakao, 平坂勝也, 東谷篤志, 東端晃, 小林剛, 曽我部正博, 武田伸一 and Takeshi Nikawa : 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, May 2018.
20.	Reiko Nakao, 榛葉繁紀 and 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, Mar. 2018.
21.	Yukari Miki, Takayuki Uchida, Yuki Kimori, Yoshihiro Sakashita, Ayako Maita, Reiko Nakao, 小林剛, 東谷篤志, 石原直忠, 武田伸一, 曽我部正博 and Takeshi Nikawa : 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, Nov. 2017.
22.	Reiko Nakao, 榛葉繁紀 and 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, Sep. 2017.
23.	Takayuki Uchida, Ayako Maita, Reiko Nakao, 小林剛, 東谷篤志, 石原直忠, 武田伸一, 曽我部正博 and Takeshi Nikawa : 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, Aug. 2017.
24.	Miyuki Ninomiya, Yuki Kimori, Marina Takagi, Kurumi Ida, Hikaru Kishimoto, Erika Takatsu, 石田祐子, 加藤健, Arisa Ochi, Takayuki Uchida, Ayako Maita, Tomoki Abe, Shigetada Kondo, Reiko Nakao, Katsuya Hirasaka and Takeshi Nikawa : 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, May 2017.
25.	Reiko Nakao, 岡内宏樹, 橋本千秋 and 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, May 2017.
26.	Takayuki Uchida, Yuki Kimori, Miyuki Ninomiya, Yoshihiro Sakashita, Tomoki Abe, Ayako Maita, Reiko Nakao, Katsuya Hirasaka, 東谷篤志, 小林剛, 曽我部正博, 武田伸一 and Takeshi Nikawa : 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, May 2017.
27.	Yuki Kimori, Miyuki Ninomiya, Chika Aihara, Yoshihiro Sakashita, Takayuki Uchida, Tomoki Abe, Reiko Nakao, Ayako Maita, Shigetada Kondo and Takeshi Nikawa : 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, May 2017.
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, Takayuki Uchida, Ayako Maita, Tomoki Abe, Shigetada Kondo, Reiko Nakao, Katsuya Hirasaka and Takeshi Nikawa : 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, Nov. 2016.

Et cetera, Workshop:

1.	Takeshi Nikawa, Takayuki Uchida, Ayako Maita, Reiko Nakao, Katsuya Hirasaka, 小林剛, 曽我部正博, 東谷篤志 and 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, Dec. 2018.
2.	Takeshi Nikawa, Takayuki Uchida, Ayako Maita, Reiko Nakao, 小林剛, 曽我部正博 and 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, Dec. 2017.
3.	Takeshi Nikawa, Takayuki Uchida, Ayako Maita and Reiko Nakao : 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, Jun. 2017.

Grants-in-Aid for Scientific Research (KAKEN Grants Database @ NII.ac.jp)

Understanding how bear serum slows down biological clock and metabolism for energy saving in skeletal muscle (Project/Area Number: 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 (Project/Area Number: 18K10994 )
Response of skeletal muscle in mice and hamster to ketogenic diet feeding (Project/Area Number: 15K16499 )
Investigating potential relationship between circadian clodk and skeletal muscle atrophy. (Project/Area Number: 24620015 )
Search by Researcher Number (20582696)

Associate Professor : Nakao, Reiko

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Grants-in-Aid for Scientific Research (KAKEN Grants Database @ NII.ac.jp)