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miR-34c-5p 对 C2C12 肌管钠、钾和钙通道电流的影响。

Effects of miR-34c-5p on Sodium, Potassium, and Calcium Channel Currents in C2C12 Myotubes.

机构信息

Department of Orthopedics and Traumatology, Peking University People's Hospital, Beijing, China.

Department of Surgery, The 517th Hospital of the People's Liberation Army, Xinzhou, Shanxi Province, China.

出版信息

Cell Mol Neurobiol. 2020 Oct;40(7):1223-1230. doi: 10.1007/s10571-020-00810-9. Epub 2020 Feb 25.

DOI:10.1007/s10571-020-00810-9
PMID:32100187
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11448787/
Abstract

The aim of this study was to investigate the effects of miR-34c-5p on the main voltage-dependent ion channels in skeletal muscle cells. This study focused on the effects of miR-34c-5p on sodium, potassium, and calcium currents in C2C12 myoblasts. The miR-34c-5p overexpression group, knockdown group, and control group were differentiated for 7 days, fused into myotubes, and used for the whole-cell patch clamp recording. Compared with the control group, the whole-cell sodium current density of the other two groups had no significant changes. In the knockdown group, the delayed rectifier potassium current density was increased (statistically significant), and the whole-cell calcium channel current density did not change. In the overexpression group, the change of rectifier potassium current density was not obvious, while the peak calcium channel current density increased (- 9.23 ± 0.95 pA/pF, n = 6 cells for the overexpression group vs. - 6.48 ± 0.64 pA/pF, n = 7 cells for the control; p < 0.05). Changes in the expression of miR-34c-5p can affect the electrophysiological characteristics of calcium and potassium voltage-gated channels in C2C12 myotubes. Overexpression of miR-34c-5p increased whole-cell L-type calcium channel current (I), while miR-34c-5p knockdown increased whole-cell delayed rectifier potassium current (I).

摘要

本研究旨在探讨 miR-34c-5p 对骨骼肌细胞主要电压依赖性离子通道的影响。本研究重点研究了 miR-34c-5p 对 C2C12 成肌细胞中钠、钾和钙电流的影响。miR-34c-5p 过表达组、敲低组和对照组分化 7 天后融合成肌管,用于全细胞膜片钳记录。与对照组相比,其他两组的全细胞钠电流密度没有明显变化。在敲低组中,延迟整流钾电流密度增加(具有统计学意义),而全细胞钙通道电流密度没有变化。在过表达组中,整流钾电流密度的变化不明显,而峰值钙通道电流密度增加(过表达组为-9.23±0.95 pA/pF,n=6 个细胞;对照组为-6.48±0.64 pA/pF,n=7 个细胞;p<0.05)。miR-34c-5p 表达的变化可以影响 C2C12 肌管中钙和钾电压门控通道的电生理特性。miR-34c-5p 的过表达增加了全细胞 L 型钙通道电流(I),而 miR-34c-5p 的敲低增加了全细胞延迟整流钾电流(I)。