2014 Fiscal Year Final Research Report
Regulation of pluripotency of skeletal muscle-derived stem cells and application to muscular diseases
| Project/Area Number |
24590363
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
General medical chemistry
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| Research Institution | Fujita Health University |
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Principal Investigator |
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| Research Collaborator |
NAKATANI Masashi 藤田保健衛生大学, 総合医科学研究所, 助教 (00421264)
HITACHI Keisuke 藤田保健衛生大学, 総合医科学研究所, 助教 (10508469)
UEZUMI Akiyoshi 藤田保健衛生大学, 総合医科学研究所, 講師 (60434594)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Keywords | 筋分化 / 筋衛星細胞 / 間葉系前駆細胞 / 脂肪分化 / 筋萎縮 / miRNA / lncRNA / 筋疾患 |
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| Outline of Final Research Achievements |
Muscle atrophies are observed both in genetic and non-genetic muscular disorders. Satellite cells play an important role in muscle repair, regeneration and muscle mass. Recently, non-myogenic mesenchymal progenitors/stem cells have been identified in muscles. They do not adopt a myogenic fate, however, they differentiate to adipocytes, fibroblasts and osteogenic cells. We have established an elegant method to purify myogenic cells and mesenchymal stem cells. Myostatin, a muscle-specific TGF-beta superfamily, is a pivotal negative regulator of muscle mass. Using myostatin knockout mice, we investigated the global microRNA expression profile. miR486, a positive regulator of IGF-1/Akt pathway, was, identified as a target of myostatin signaling. Overexpression of miR486 induced myotube hypertrophy. miR486 is one of the intermediate molecules linking myostatin signaling and the IGF-1/Akt/mTOR pathway in the regulation of skeletal muscle size.
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| Free Research Field |
分子細胞生物学
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