Myocyte-specific enhancer factor 2C: a novel target gene of miR-214-3p in suppressing angiotensin II-induced cardiomyocyte hypertrophy.
Myocyte-specific enhancer factor 2C: a novel target gene of miR-214-3p in suppressing angiotensin II-induced cardiomyocyte hypertrophy.
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心肌细胞特异性增强因子2C：miR-214-3p抑制血管紧张素II诱导的心肌细胞肥大的新靶基因
DOI：
10.1038/srep36146
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发表时间：
2016-10-31
影响因子：
4.6
通讯作者：
Shan ZX
中科院分区：
文献类型：
--
作者：
Tang CM;Liu FZ;Zhu JN;Fu YH;Lin QX;Deng CY;Hu ZQ;Yang H;Zheng XL;Cheng JD;Wu SL;Shan ZX
MicroRNA-214-3p(miR-214-3p)在心肌肥厚中的作用尚不清楚。本研究旨在探讨miR-214-3p在血管紧张素II(Ang-II)诱导的小鼠心肌肥厚中的表达及其可能的靶点。Ang-II组和TAC模型组大鼠肥厚心肌miR-214-3p表达均显著降低。心肌肥厚患者心肌miR-214-3p表达下调。在Ang-II诱导的肥大新生小鼠心肌细胞中，miR-214-3p表达上调。尾静脉注射miR-214-3P可减轻Ang-II诱导的小鼠心肌肥厚。此外，miR214-3p抑制Ang-II处理的小鼠心肌细胞心钠素和β-肌球蛋白重链的表达。心肌细胞特异性增强因子2C(MEF2C)是miR-214-3p的靶基因，在Ang-II诱导的肥大小鼠心肌和心肌细胞中表达增加。在功能上，miR214-3p模拟血管紧张素Ⅱ处理的小鼠心肌细胞，抑制心钠素和β-MHC的蛋白表达，与MEF2CsiRNA一致。核因子-κB信号通路参与了血管紧张素Ⅱ诱导的心肌细胞miR214-3p的表达。综上所述，我们的结果表明，MEF2C是miR-214-3p的一个新靶点，miR-214-3p表达的减弱可能参与了心肌肥厚中MEF2C的表达。
The role of microRNA-214-3p (miR-214-3p) in cardiac hypertrophy was not well illustrated. The present study aimed to investigate the expression and potential target of miR-214-3p in angiotensin II (Ang-II)-induced mouse cardiac hypertrophy. In mice with either Ang-II infusion or transverse aortic constriction (TAC) model, miR-214-3p expression was markedly decreased in the hypertrophic myocardium. Down-regulation of miR-214-3p was observed in the myocardium of patients with cardiac hypertrophy. Expression of miR-214-3p was upregulated in Ang-II-induced hypertrophic neonatal mouse ventricular cardiomyocytes. Cardiac hypertrophy was attenuated in Ang-II-infused mice by tail vein injection of miR-214-3p. Moreover, miR-214-3p inhibited the expression of atrial natriuretic peptide (ANP) and β-myosin heavy chain (MHC) in Ang-II-treated mouse cardiomyocytesin vitro. Myocyte-specific enhancer factor 2C (MEF2C), which was increased in Ang-II-induced hypertrophic mouse myocardium and cardiomyocytes, was identified as a target gene of miR-214-3p. Functionally, miR-214-3p mimic, consistent with MEF2C siRNA, inhibited cell size increase and protein expression of ANP and β-MHC in Ang-II-treated mouse cardiomyocytes. The NF-κB signal pathway was verified to mediate Ang-II-induced miR-214-3p expression in cardiomyocytes. Taken together, our results revealed that MEF2C is a novel target of miR-214-3p, and attenuation of miR-214-3p expression may contribute to MEF2Cexpressionin cardiac hypertrophy.
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