| Project/Area Number |
15K08188
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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 |
General physiology
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| Research Institution | Tokyo Medical University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
井上 華 東京医科大学, 医学部, 講師 (20390700)
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| Project Period (FY) |
2015-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2017: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | マグネシウム / TRPM7 / 心筋細胞 / 細胞内マグネシウムイオン濃度 / ラット心室筋細胞 / 生理的Mgチャネル / ナルトリベン / マグネシウムイオン / 細胞内マグネシウム恒常性 / ラット心室筋 / 初代培養細胞 / SLC41A1 / 組換えアデノウイルス |
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| Outline of Final Research Achievements |
In rat ventricular myocytes, Mg2+ influx rate was increased by naltriben which activates TRPM7 channel, in a concentration-dependent manner. This effect is similar to that reported for TRPM7.
H9c2 cells derived from the rat heart were transfected with shRNA of TRPM7 or non-targeting shRNA (control). Intracellular free magnesium concentration ([Mg2+]i) of TRPM7 knockdown cells was not significantly different from that of control cells. The addition of extracellular Mg2+ raised [Mg2+]i in control cells. The increment in [Mg2+]i of TRPM7 knockdown cells was significantly smaller than that of control cells. In conclusion, it is suggested that TRPM7 knockdown decreases the rate of Mg2+ influx in H9c2 myocytes, although cytoplasmic Mg2+ homeostasis appears to be still maintained at normal [Mg2+]o.
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| Academic Significance and Societal Importance of the Research Achievements |
マグネシウム(Mg)イオンは細胞内で300以上の反応の補酵素として働き、代謝やDNA合成でも重要な役割を担う。心筋細胞内のMg濃度調節系の破綻は心不全や不整脈を引き起こす。このため、細胞内Mg濃度は一定に維持されているが、調節機構はまだ解明されていない。調節を担う分子の解明は、創薬へと発展し、治療に繋がっていく。本研究ではラット心室筋細胞へのMg流入が促進される時に、TRPM7が流入経路となることを示唆した。
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