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首页> 外文期刊>Molecules and cells >MicroRNA-206 Protects against Myocardial Ischaemia-Reperfusion Injury in Rats by Targeting Gadd45β
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MicroRNA-206 Protects against Myocardial Ischaemia-Reperfusion Injury in Rats by Targeting Gadd45β

机译:MicroRNA-206通过靶向Gadd45β预防大鼠心肌缺血-再灌注损伤

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MicroRNAs are widely involved in the pathogenesis of cardiovascular diseases through regulating gene expression via translational inhibition or degradation of their target mRNAs. Recent studies have indicated a critical role of microRNA-206 in myocardial ischaemia-reperfusion (I/R) injury. However, the function of miR-206 in myocardial I/R injury is currently unclear. The present study was aimed to identify the specific role of miR-206 in myocardial I/R injury and explore the underlying molecular mechanism. Our results revealed that the expression level of miR-206 was significantly decreased both in rat I/R group and H9c2 cells subjected to hypoxia/reoxygenation (H/R) compared with the corresponding control. Overexpression of miR-206 observably decreased infarct size and inhibited the cardiomyocyte apoptosis induced by I/R injury. Furthermore, bioinformatics analysis, luciferase activity and western blot assay proved that Gadd45β (growth arrest DNA damage-inducible gene 45β) was a direct target gene of miR- 206. In addition, the expression of pro-apoptotic-related genes, such as p53, Bax and cleaved caspase3, was decreased in association with the down-regulation of Gadd45β. In summary, this study demonstrates that miR-206 could protect against myocardial I/R injury by targeting Gadd45β.
机译:MicroRNA通过翻译抑制或目标mRNA的降解来调控基因表达,从而广泛参与心血管疾病的发病机制。最近的研究表明,microRNA-206在心肌缺血再灌注(I / R)损伤中具有关键作用。但是,目前尚不清楚miR-206在心肌I / R损伤中的功能。本研究旨在确定miR-206在心肌I / R损伤中的特定作用,并探讨其潜在的分子机制。我们的结果表明,与相应的对照组相比,在大鼠I / R组和经历过缺氧/复氧(H / R)的H9c2细胞中,miR-206的表达水平均明显降低。 miR-206的过表达可明显减少梗死面积并抑制I / R损伤诱导的心肌细胞凋亡。此外,生物信息学分析,荧光素酶活性和蛋白质印迹试验证明,Gadd45β(生长停滞DNA损伤诱导基因45β)是miR-206的直接靶基因。此外,促凋亡相关基因(如p53)的表达,Bax和裂解的caspase3,与Gadd45β的下调有关而降低。总而言之,这项研究表明miR-206可通过靶向Gadd45β来预防心肌I / R损伤。

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