| Project/Area Number |
23591061
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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 |
Circulatory organs internal medicine
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| Research Institution | Kitasato University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
NIWANO Hiroe 玉川大学, 教育学部, 教授 (00293233)
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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 |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2012: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2011: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | Kv1.3 / Kir2.1 / 電気的リモデリング / 構造的リモデリング / 心不全 / 不整脈 |
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| Research Abstract |
The down-regulation of Ito channel in failure heart will prolong the action potential duration and it accelerates the calcium over-load induced myocardial injury. This study aimed to induce reverse remodeling by removing this vicious circle via normalization of action potential. In our preceding study, we tried to transfect Ito channel directly to the myocyte by using Kv4.2, Kv4.3 and KChIP2 transfection, but enough amount of expression of these molecules myocyte could not be achieved, then we utilized fibroblast transplantation method in this study. We transfected Kv1.3+Kir2.1 into the fibroblast, then tried to transplant them into cardiac tissue. They will construct electrical connection to the myocytes and the action potential will be shortened as well as decrease in calcium over-load in the failure myocytes. In the recent protocol, we succeeded to transfect Kv1.3 to the fibroblast but the stable expression of Kir2.1 was not achieved during the scheduled study period.
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