| Project/Area Number |
17K15615
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Pathological medical chemistry
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| Research Institution | Mie University |
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Principal Investigator |
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| Project Period (FY) |
2017-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2019: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2018: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2017: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
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| Keywords | 中間径フィラメント / 筋肉 / 心筋 / 骨格筋 / 筋再生 / デスミン / Desmin / 細胞分裂 / 老化 / 早老症 / 平滑筋 / 分子病態学 / 生理学 / 発生学 / 循環器 |
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| Outline of Final Research Achievements |
To understand the physiological significance of mitotic phosphorylation of muscle specific intermediate filament desmin, we generated mitotic desmin phosphorylation defective mice (DES SA/SA mice). Compare to wild type mice, DES SA/SA mice were no difference of appearance. However, in heart muscle tissue, DES SA/SA mice showed decrease of desmin expression in Z band area except intercalated disc. Therefore, we need to clarify heart function in the future. In skeletal muscle tissue, when we induced acute muscle injury by glycerol injection, DES SA/SA mice were injured broadly and delayed muscle regeneration. In future, we will work on solution of detail mechanism with regards to pre-existing muscle tissue homeostasis and abnormal cell division of muscle stem cell which is called satellite cell.
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| Academic Significance and Societal Importance of the Research Achievements |
デスミンリン酸化の生理的意義を明らかにすることで、細胞同士の融合で多核となる筋組織の形成メカニズムの詳細を知ることができる。これを元に筋組織の老化や障害に対する効率の良い筋肉再生法の開発に貢献することが期待できる。またヒトにおいてもデスミンは遺伝的変異が原因によるミオパチーが存在し、リン酸化部位の変異もいくつか知られている。そのため、デスミンの遺伝子変異によるミオパチーの治療法の開発にも本研究で獲られる知見が役立つと考える。
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