2011 Fiscal Year Final Research Report
Molecular mechanisms of muscle mass regulation : Identification of a novel protease involved in myostatin activation.
| Project/Area Number |
21500632
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Sports science
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| Research Institution | The University of Tokushima |
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Principal Investigator |
OKUMURA Yuushi 徳島大学, 大学院・ヘルスバイオサイエンス研究部, 准教授 (70294725)
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| Co-Investigator(Kenkyū-buntansha) |
NIKAWA Takeshi 徳島大学, 大学院・ヘルスバイオサイエンス研究部, 教授 (20263824)
NAKAYA Yutaka 徳島大学, 大学院・ヘルスバイオサイエンス研究部, 教授 (50136222)
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| Project Period (FY) |
2009 – 2011
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| Keywords | 筋量決定サイトカイン / 膜結合型プロテアーゼ / 筋萎縮 |
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| Research Abstract |
Muscle mass was decreased by disuse and this condition was thought to regulate by myostatin. Myostatin, a member of TGF-βsuperfamily, has been well characterized as a negative regulator of muscle growth and development. Myostatin is synthesized as a precursor protein and activated by cellular proteases on the cell surface. In this study, as candidate processing proteases for myostatin activation, we could identify a novel protease, MSPL(type II transmembrane serine protease). Interestingly, treatment with MSPL inhibitor to the cells expressing myostatin revealed that a part of it could start differentiation. This result suggested that myostatin activation was regulated by the regulation of MSPL enzymatic activity. To confirm the involvement of MSPL for myostatin activation in vivo, we generated MSPL deficient(MSPL-/-) mice. Unfortunately, from the studies of MSPL-/-mice in unloading condition, no significant differences were observed in the wet weight muscle volume in MSPL-/-mouse compared than in MSPL+/+(Wild-type) mouse(n=1). However, we need to confirm this result by repeating experiments(at least n> 3). The expression and activation of myostatin in MSPL-/-mice are currently being investigated.
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