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目的:研究心脏成纤维细胞(CFs)膜上的TRPM7通道的电生理特性。方法:将分离培养出来的乳鼠CFs用6种不同浓度的血管紧张素Ⅱ(AngⅡ)干预至12h,分别测量各组胶原蛋白的表达水平,从而挑选出最佳诱导纤维化的AngⅡ浓度,最佳浓度的AngⅡ分别将CFs干预至5个不同的时间,记录相应的CFs膜上的TRPM7电流及各组的胶原蛋白水平。结果:诱导心脏纤维化最大的AngⅡ浓度是1nmol/L,最佳诱导纤维化浓度干预0,6,12,24,48h后CFs的TRPM7与胶原蛋白Ⅲ的表达水平最初升高,于12h达到最高水平,之后呈现递减水平,且在CFs膜上记录到的TRPM7内外向电流也呈现相应的先增加后降低趋势,与两种蛋白的表达水平正相关。结论:CFs膜上的TRPM7电流在AngⅡ的作用下,呈现先增加后减少的趋势,是AngⅡ介导CFs增殖与凋亡从而导致心脏纤维化的重要途径之一。
Objective: To investigate the electrophysiological properties of TRPM7 channels on cardiac fibroblasts (CFs). Methods: The isolated CFs from neonatal rats were treated with six different concentrations of angiotensin Ⅱ (AngⅡ) for 12 h. The expression of collagen in each group was measured to select the optimal concentration of AngⅡ for inducing fibrosis The best concentrations of AngⅡinterfering CFs to 5 different time, recording the TRPM7 current and the collagen level of the corresponding CFs. Results: The maximum AngII concentration induced by cardiac fibrosis was 1 nmol / L. The expression of TRPM7 and collagen Ⅲ in CFs was increased at the optimal concentration of fibrosis intervention at 0, 6, 12, 24 and 48 h, reaching the highest at 12 h Level, and then showed a decreasing level, and the inward and outward currents of TRPM7 recorded on CFs membrane also increased correspondingly firstly and then decreased, positively correlated with the expression level of the two proteins. CONCLUSION: The TRPM7 current on CFs membrane first increases and then decreases under the action of AngⅡ, which is one of the important pathways that Ang Ⅱ mediates the proliferation and apoptosis of CFs and leads to cardiac fibrosis.