Wang Yongyi, Men Min, Yang Wengang, Zheng Hui, Xue Song
Department of Cardiovascular Surgery, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Cell Physiol Biochem. 2015;36(1):179-90. doi: 10.1159/000374062. Epub 2015 Apr 30.
Various miRNAs have been shown to participate in cardiac ischemia/reperfusion injury (I/R). miR-31 was identified as the most strikingly upregulated miRNA after acute myocardial infarction; therefore, the underlying role and mechanism of miR-31 in cardiac I/R was investigated.
miR-31 expression was detected after cardiac I/R in mice. The cardioprotective effect of miR-31 downregulation was assessed in vitro and in vivo. The functional target gene and its downstream molecule were determined.
miR-31 expression increased after I/R. miR-31 downregulation increased cell viability and SOD activity and decreased LDH activity and MDA content in vitro. Additionally, miR-31 downregulation alleviated myocardial infarct size in vivo. PKCε was identified as the functional target gene of miR-31, and NFκB was identified as its downstream molecule that was involved in the miR-31-mediated cardioprotective effect.
miR-31 expression increased throughout the cardiac I/R process, and miR-31 downregulation induced a cardioprotective effect via a miR-31/PKCε/NFκB-dependent pathway.
多种微小RNA（miRNA）已被证明参与心脏缺血/再灌注损伤（I/R）。miR-31被确定为急性心肌梗死后上调最为显著的miRNA；因此，对miR-31在心脏I/R中的潜在作用及机制进行了研究。
检测小鼠心脏I/R后miR-31的表达。在体外和体内评估下调miR-31的心脏保护作用。确定功能性靶基因及其下游分子。
I/R后miR-31表达增加。下调miR-31可增加体外细胞活力和超氧化物歧化酶（SOD）活性，降低乳酸脱氢酶（LDH）活性和丙二醛（MDA）含量。此外，下调miR-31可减轻体内心肌梗死面积。蛋白激酶Cε（PKCε）被确定为miR-31的功能性靶基因，核因子κB（NFκB）被确定为参与miR-31介导的心脏保护作用的下游分子。
在整个心脏I/R过程中miR-31表达增加，下调miR-31通过miR-31/PKCε/NFκB依赖性途径诱导心脏保护作用。
