title: MicroRNA-22 targeting CBP protects against myocardial ischemia-reperfusion injury through anti-apoptosis in rats.
abstract: MicroRNAs are extensively involved in the pathogenesis of major cardiovascular diseases by suppressing target gene expression. Recent studies have reported that microRNA-22 (miR-22) may be implicated in ischemia-reperfusion (I/R) induced myocardial injury. However, the specific function of miR-22 in myocardial I/R injury is far from clear nowadays. The present study was designed to determine the role of miR-22 in myocardial I/R injury and investigate the underlying cardio-protective mechanism. The rat myocardial I/R injury model was induced by occluding the left anterior descending coronary artery for 30 min followed by 12 h reperfusion. As predicted, adenovirus-mediated miR-22 overexpression markedly reduced the release of creatine kinase and lactate dehydrogenase, infarct size and cardiomyocytes apoptosis. Moreover, CREB binding protein (CBP) as a potential miR-22 target by bioinformatics was significantly inhibited after miR-22 transfection. We also found that p53 acetylation activity, pro-apoptotic related genes Bax and p21 levels were all decreased associated with the down-regulation of CBP. In conclusion, our data demonstrate that miR-22 could inhibit apoptosis of cardiomyocytes through one of its targets, CBP. Thus, miR-22 may constitute a new therapeutic target for the prevention of myocardial I/R injury.
authors: Department of Cardiology, The First College of Clinical Medical Sciences, China Three Gorges University, Yichang, 443000, Hubei, China.
authors: Jian
authors: J
authors: Yang
authors: Lihua
authors: L
authors: Chen
authors: Jun
authors: J
authors: Yang
authors: Jiawang
authors: J
authors: Ding
authors: Song
authors: S
authors: Li
authors: Hui
authors: H
authors: Wu
authors: Jing
authors: J
authors: Zhang
authors: Zhixing
authors: Z
authors: Fan
authors: Wusong
authors: W
authors: Dong
authors: Xinxin
authors: X
authors: Li
mesh_terms: D000107:Acetylation; D000818:Animals; D017209:Apoptosis; D001483:Base Sequence; D001665:Binding Sites; D050882:CREB-Binding Protein / Q000235:genetics* / Q000378:metabolism; D003402:Creatine Kinase / Q000097:blood; D015536:Down-Regulation; D015870:Gene Expression; D007770:L-Lactate Dehydrogenase / Q000097:blood; D008297:Male; D035683:MicroRNAs / Q000235:genetics*; D015428:Myocardial Reperfusion Injury / Q000378:metabolism* / Q000473:pathology; D009206:Myocardium / Q000473:pathology; D032383:Myocytes, Cardiac / Q000502:physiology; D011499:Protein Processing, Post-Translational; D034622:RNA Interference; D051381:Rats; D017207:Rats, Sprague-Dawley; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism
chemical_list: C580892:MIRN22 microRNA, rat; D035683:MicroRNAs; D016159:Tumor Suppressor Protein p53; D007770:L-Lactate Dehydrogenase; D050882:CREB-Binding Protein; C494365:Crebbp protein, rat; D003402:Creatine Kinase