MicroRNA-135a Regulates Apoptosis Induced by Hydrogen Peroxide in Rat Cardiomyoblast Cells.
MicroRNA-135a Regulates Apoptosis Induced by Hydrogen Peroxide in Rat Cardiomyoblast Cells.
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MicroRNA-135a 调节过氧化氢诱导的大鼠成肌细胞细胞凋亡
DOI：
10.7150/ijbs.16769
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发表时间：
2017
影响因子：
9.2
通讯作者：
Liu B
中科院分区：
文献类型：
--
作者：
Liu N;Shi YF;Diao HY;Li YX;Cui Y;Song XJ;Tian X;Li TY;Liu B
氧化应激和细胞凋亡是缺血性心脏病最重要的病理特征。最近的研究表明microRNAs（miRs）在细胞凋亡中起着重要的作用。然而，miRs是否可能在缺血性心脏病中调节B细胞淋巴瘤-2（Bcl-2）蛋白的凋亡仍不清楚。因此，本研究的目的是证实microRNA-135 a（miR-135 a）在过氧化氢（H2 O2）诱导的大鼠心肌细胞H9 c2氧化应激损伤中的调节作用。为此，我们分析了H2 O2处理对大鼠心肌细胞中miR-135 a表达的影响。此外，我们分别使用模拟物和抑制剂上调和抑制miR-135 a，并检查对细胞活力和凋亡相关蛋白的影响。我们观察到miR-135 a在H2 O2处理的大鼠心肌细胞中显著上调。过表达miR-135 a可阻断Bcl-2蛋白的表达，增强H2 O2诱导的细胞凋亡，抑制miR-135 a可恢复Bcl-2蛋白的表达。有趣的是，miR-135 a抑制并没有减弱H2 O2诱导的凋亡与Bcl-2敲低。本研究结果表明，miR-135 a通过靶向Bcl-2调节H2 O2诱导的H9 c2细胞凋亡，miR-135 a可能成为缺血性心脏病治疗的新靶点。
Oxidative stress and apoptosis are the most important pathologic features of ischemic heart disease. Recent research has indicated that microRNAs (miRs) play an essential role in apoptosis. However, whether miRs might regulate B cell lymphoma-2 (Bcl-2) protein in apoptosis during ischemic heart disease is still unclear. The aim of this study, therefore, was to confirm the regulation of microRNA-135a (miR-135a) in oxidative stress injuries induced by hydrogen peroxide (H2O2) in rat cardiomyoblast cells H9c2. To this end, we analyzed the effects of H2O2 treatment on miR-135a expression in rat cardiomyocytes. Furthermore, we upregulated and inhibited miR-135a using mimics and inhibitors, respectively, and examined the effects on cell viability and apoptosis-related proteins. We observed that miR-135a was markedly up-regulated under H2O2 treatment in rat cardiomyoblast cells. Overexpression of miR-135a blocked the Bcl-2 protein and enhanced the apoptosis induced by H2O2, and miR-135a inhibition restored Bcl-2 protein expression. Interestingly, miR-135a inhibition did not attenuate H2O2-induced apoptosis with Bcl-2 knockdown. The results of the present study indicate that miR-135a regulates H2O2-induced apoptosis in H9c2 cells via targeting Bcl-2, and that miR-135a may be a novel therapeutic target for ischemic heart disease.