TRPM7 silencing attenuates Mg2+ influx in cardiac myoblasts, H9c2 cells

• Published in: The journal of physiological sciences Vol. 70; no. 1; pp. 1 - 47
• Main Authors: Tashiro, Michiko, Konishi, Masato, Kobayashi, Ryo, Inoue, Hana, Yokoyama, Utako
• Format: Journal Article
• Language: English
• Published: Heidelberg Springer 07.10.2020; BioMed Central
• Subjects: Antibodies; Calcium; Efficiency; Ethylenediaminetetraacetic acid; Fluorescent indicators; Homeostasis; Magnesium; Myoblasts; Physiology; Scientific equipment and supplies industry; Short Communication; Transient receptor potential proteins; United States; United States > US
• DOI: 10.1186/s12576-020-00772-z
• ISSN: 1880-6546

TRPM7, a member of the melastatin subfamily of transient receptor potential channels, is suggested to be a potential candidate for a physiological Mg 2+ channel. However, there is no direct evidence of Mg 2+ permeation through endogenous TRPM7. To determine the physiological roles of TRPM7 in intracellular Mg 2+ homeostasis, we measured the cytoplasmic free Mg 2+ concentration ([Mg 2+ ] i ) in TRPM7-silenced H9c2 cells. [Mg 2+ ] i was measured in a cluster of 8–10 cells using the fluorescent indicator, furaptra. TRPM7 silencing did not change [Mg 2+ ] i in Ca 2+ -free Tyrode’s solution containing 1 mM Mg 2+ . Increasing the extracellular Mg 2+ to 92.5 mM raised [Mg 2+ ] i in control cells (1.56 ± 0.19 mM) at 30 min, while this effect was significantly attenuated in TRPM7-silenced cells (1.12 ± 0.07 mM). The Mg 2+ efflux driven by Na + gradient was unaffected by TRPM7 silencing. These results suggest that TRPM7 regulates the rate of Mg 2+ influx in H9c2 cells, although cytoplasmic Mg 2+ homeostasis at basal conditions is unaffected by TRPM7 silencing.