| Project/Area Number |
16K18994
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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 |
General physiology
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| Research Institution | Japan Aerospace EXploration Agency |
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Principal Investigator |
Ohira Takashi 国立研究開発法人宇宙航空研究開発機構, 有人宇宙技術部門, 研究開発員 (40633532)
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| Project Period (FY) |
2016-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2017: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2016: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 骨格筋 / 坐骨神経切除 / カルシウムハンドリング / サルコリピン |
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| Outline of Final Research Achievements |
Sarcolipin (SLN) and Phospholamban (PLN) inhibit the activity of sarco/endoplasmic reticulum Ca2+-ATPase (SERCA). SLN and PLN proteins markedly increased in mouse soleus (Sol) muscle following denervation. The increase in PLN, but not SLN, protein was also observed in denervated extensor digitorum longus (EDL) muscle. However, the denervation-induced PLN level in EDL muscle was lower than Sol muscle. At the same time, increase in SERCA2 and decrease in SERCA1 were observed in denervated Sol and EDL muscles, respectively. These changes were become prominent according to decrease in the muscle wet weights. Increases in SLN and/or PLN were likely to be contributed to enhance the cytosolic calcium concentration in atrophying muscle fibers further, rather than trigger the elevation of the cytosolic calcium concentration.
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| Academic Significance and Societal Importance of the Research Achievements |
本研究では、マウスのヒラメ筋および長趾伸筋において坐骨神経切除後の筋湿重量の減少と並行してＳＥＲＣＡの機能抑制タンパク質が増加することを確認した。この結果から、両筋におけるＳＥＲＣＡを介した細胞質から筋小胞体へのカルシウムイオンの取り込み能は筋萎縮の進行とともに低下したことが考えられる。したがって、ＳＥＲＣＡの機能抑制タンパク質の増加は、筋萎縮開始時に筋細胞質内のカルシウムイオン濃度を上昇させる要因ではなく、筋萎縮進行中に筋細胞質内のカルシウムイオン濃度を高いまま維持する、またはさらに上昇させる要因となっていることが示唆される。
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