血管紧张素 II通过增加miR-21表达促进心脏成纤维细胞胶原合成

目的 探讨血管紧张素II（AngII）促进心脏成纤维细胞胶原合成的分子机制，初步分析miR-21在其中发挥的作用。方法 使用SD大鼠心脏组织分离培养原代成纤维细胞；分别使用0、0.1、0.2和0.4 μmol/L的AngII刺激细胞36 h，qRT-PCR检测胶原（Col1a1和Col3a1）和miR-21的表达变化；使用miR-21抑制物（miR-21 inhibitor）转染细胞，AngII刺激后，qRT-PCR检测Col1a1和Col3a1的表达。结果 镜下观察和标志物分子检测表明心脏成纤维细胞培养成功。在AngII刺激下，Col1a1、Col3a1和miR-21均呈剂量依赖性表达增加(P<0.05)。使用miR-21抑制物能显著降低Ang II刺激下Col1a1和Col3a1的表达升高(P<0.05)。结论 AngII能增加心脏成纤维细胞的胶原合成，其相关机制可能部分通过miR-21相关信号来介导。

Angiotensin II promotes collagen synthesis in cardiac fibroblast via miR-21

AIM To explore the role of angiotensin II (AngII) in the collagen synthesis of cardiac fibroblasts and the putative involvement of miR-21. METHODSPrimary cardiac fibroblast cells were isolated from Sprague Dawley rats and the cells were treated with 0, 0.1, 0.2 and 0.4 μmol/L AngII for 36 h. Expressions of Col1a1, Col3a1 and miR21 were analyzed by qRT-PCR. MiR-21 was knocked down by transfected miR-21 inhibitor into cardiac fibroblast cells. RESULTSCardiac fibroblast cells were successfully isolated and cultured as seen morphologically under the microscope and expression of the markers. Upon AngII treatment, expressions of Col1a1, Col3a1 and miR21 increased in a dose-dependent manner. miR21 inhibitor markedly blocked the induction of Col1a1 and Col3a1 by AngII. CONCLUSIONAngII induces collagen synthesis in which induction of miR-21 might be essential.