2018 Fiscal Year Final Research Report
Elucidation of the mechanism of arrhythmia in cardiac ischemia-reperfusion injury by imaging technology
| Project/Area Number |
16K01356
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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 |
Biomedical engineering/Biomaterial science and engineering
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| Research Institution | Okayama University |
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Principal Investigator |
Takahashi Ken 岡山大学, 医歯薬学総合研究科, 助教 (50432258)
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| Research Collaborator |
Naruse Keiji
Wang Chen
Miyaji Takaaki
Wei Heng
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| Project Period (FY) |
2016-04-01 – 2019-03-31
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| Keywords | 心筋梗塞 / 虚血再灌流障害 / MALDI-TOF / TRPM4 / CRISPR/Cas9 / ミトコンドリア膜電位 / 細胞内ATP濃度 / iPS細胞 |
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| Outline of Final Research Achievements |
Calcium sensitive dye Fluo4 was successfully perfused into the isolated rat heart in ex-vivo condition.
MALDI imaging was performed to construct a 3D map of TRPM4 protein in the heart, which allowed simultaneous mapping of more than 57 proteins at 100 μm resolution.
We developed a new experiment system using human iPS cardiomyocytes and models of ischemia-reperfusion injury, based on the previous system using rat heart and cardiomyocytes. Pretreatment of an inhibitor of TRPM4 channel protected the iPS cardiomyocytes from cell injury under ischemia-reperfusion condition. This result suggests that TRPM4 channel is involved in ischemia-reperfusion injury in human as well.
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| Free Research Field |
生体医工学、心臓生理学
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| Academic Significance and Societal Importance of the Research Achievements |
心機能に関し、ヒトとラット・マウスとの間の違いが従来より指摘されている。従って、本研究でヒト由来のiPS心筋細胞を用いる心臓虚血再灌流障害の実験系を確立した意義は極めて大きい。本研究をさらに進めることにより、ヒトの心筋梗塞の予防法開発につながることが期待される。
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