| Project/Area Number |
23790255
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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 | Jikei University School of Medicine |
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Principal Investigator |
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥3,250,000 (Direct Cost: ¥2,500,000、Indirect Cost: ¥750,000)
Fiscal Year 2013: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2012: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2011: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
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| Keywords | 細胞内Ca2+動態 / 心筋筋小胞体 / ATP依存性筋小胞体Ca2+ポンプ / 国際情報交換 / 国際情報交流 |
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| Research Abstract |
We investigated the role of the alteration of sarcoplasmic reticulum (SR) which is known to be a cause of cardiac dysfunction in failing heart. We used saponin-treated thin trabeculae obtained from mice hearts with overexpression of SR-Ca2+ ATPase (SERCA-TG) and sarcolipin (SLN-TG), respectively. Ca2+ uptake rate was faster in SERCA-TG and slower in SLN-TG. Maximal Ca2+ content, Ca2+ induced Ca2+ release and Ca2+ leak were not altered in SERCA-TG and SLN-TG. In the papillary muscle experiment using Ca2+ sensitive photoprotein aequorin, peak tension and peak amplitude of Ca2+ transient were increased in SERCA-TG and decreased in SLN-TG. Relaxation time of tension and decline of Ca2+ transient were accelerated in SERCA-TG and prolonged in SLN-TG. Thus, we concluded that selective modulation of Ca2+ uptake into SR influenced the amplitude and time course of Ca2+ transient and tension, however, it did not influence maximal Ca2+ content, Ca2+ induced Ca2+ release and Ca2+ leak of SR.
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