Journal
MOLECULAR BIOLOGY REPORTS
Volume 41, Issue 1, Pages 555-561Publisher
SPRINGER
DOI: 10.1007/s11033-013-2891-x
Keywords
MicroRNAs; Reperfusion injury; CREB binding protein; Apoptosis; Cardiomyocytes
Categories
Funding
- National Natural Science Foundation of China [81200088, 81201458]
- Natural Science Foundation of Yichang city, China [A12301-01]
Ask authors/readers for more resources
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
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available