| Project/Area Number |
17K19940
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| Research Category |
Grant-in-Aid for Challenging Research (Exploratory)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Health science and related fields
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| Research Institution | Fukuoka University |
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Principal Investigator |
Higaki Yasuki 福岡大学, スポーツ科学部, 教授 (10228702)
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| Co-Investigator(Kenkyū-buntansha) |
兼岡 秀俊 福岡大学, 医学部, 教授 (20161169)
北嶋 康雄 熊本大学, 発生医学研究所, 助教 (70734416)
安野 哲彦 福岡大学, 医学部, 准教授 (80551994)
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| Project Period (FY) |
2017-06-30 – 2021-03-31
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| Project Status |
Completed (Fiscal Year 2020)
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| Budget Amount *help |
¥6,500,000 (Direct Cost: ¥5,000,000、Indirect Cost: ¥1,500,000)
Fiscal Year 2019: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2018: ¥2,860,000 (Direct Cost: ¥2,200,000、Indirect Cost: ¥660,000)
Fiscal Year 2017: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | サテライト細胞 / 一酸化窒素合成酵素 / DNAメチル化 / メチル化 / 幹細胞 / 筋サテライト細胞 / 筋幹細胞 / ミトコンドリア |
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| Outline of Final Research Achievements |
DNA methylation may play an important role in regulating gene expression in skeletal muscle to adapt to physical activity and inactivity. Neuronal nitric oxide synthase (nNOS) in skeletal muscle is a key regulator of skeletal muscle mass; however, it is unclear whether nNOS expression is regulated by DNA methylation. While, muscle satellite cells, which are stem cells of skeletal muscle, play an important role in muscle regeneration and repair. We therefore determined nNOS expression and DNA methylation in muscle satellite cells in injured muscle-derived muscle satellite cells (CTX). The number of Pax7+ cells were significantly lower in CTX group than that in control group. The number of Pax7+nNOS double-positive cells and nNOS gene expression levels in CTX group were comparable to those in control group. These results suggest that CTX induced injury does not affect nNOS expression in muscle satellite cells.
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| Academic Significance and Societal Importance of the Research Achievements |
骨格筋は、力学的負荷により肥大し、脱負荷により萎縮する。健康寿命の延伸には、生涯にわたり骨格筋量をいかに維持するか、そして代謝を含めた機能をいかに高めるか、重要である。本研究は、筋量を制御する因子の一つである神経型一酸化窒素合成酵素のエピジェネティックな遺伝子修飾を明らかにした。高齢社会におけるフレイル・サルコペニアの課題を解決するためのエビデンスの一つになったものと考えている。
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