氧化应激
免疫印迹
细胞凋亡
活性氧
丙二醛
基因敲除
超氧化物歧化酶
细胞生物学
流式细胞术
化学
细胞内
分子生物学
生物
生物化学
基因
作者
Feng Liu,Han Zhang,Zhe Zhang,Yanjiao Lu,Xueli Lu
标识
DOI:10.1016/j.ejphar.2019.172668
摘要
Oxidative stress injury, inducing cardiomyocyte injury, is the major denominator of many cardiovascular diseases. In present study, we aimed to explore the molecular mechanism of microRNA-208a (miR-208a) in oxidative stress-induced cardiomyocyte injury. In this study, hydrogen peroxide (H2O2)-induced injury in H9c2 and AC16 cardiomyocytes was used as a model of myocardial injury. The pro-apoptosis potential and mechanism of miR-208a for oxidative injury were evaluated by MTT, flow cytometry, qRT-PCR and Western blot assays. Intracellular reactive oxygen species and detection of lactate dehydrogenase (LDH), malondialdehyde (MDA), and superoxide dismutase (SOD) were performed to analyze the effect of miR-208a on H2O2-induced injury in H9c2 cardiomyocytes. The association between miR-208a and activated protein C (APC) was confirmed by luciferase reporter and RIP assays. We foundthatmiR-208a mimic aggravated H2O2-induced apoptosis and oxidative injury in cardiomyocytes, while miR-208a inhibitor hadan inverse effect. APC was a target gene of miR-208a and miR-208a negatively regulated the expression of APC. APC reduced H2O2-induced injury in H9c2 cardiomyocytes. Knockdown of APC attenuated the inhibitiveeffect of miR-208a inhibitor on H2O2-induced injuryin H9c2 cardiomyocytes. We concluded thatmiR-208a could aggravate H2O2-induced injury in H9c2 cardiomyocytes by targeting APC. A new signaling pathway miR-208a/APC was first observed in myocardial injury.
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