Involvement of TRPM7 in intracellular magnesium homeostasis

2018 Fiscal Year Final Research Report

• Project/Area Number: 15K08188
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: General physiology
• Research Institution: Tokyo Medical University
• Principal Investigator: Tashiro Michiko 東京医科大学, 医学部, 講師 (20398762)
• Co-Investigator(Kenkyū-buntansha): 井上 華 東京医科大学, 医学部, 講師 (20390700)
• Project Period (FY): 2015-04-01 – 2019-03-31
• Keywords: マグネシウム / TRPM7 / 心筋細胞

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.

Free Research Field

細胞生理学

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。