| Literature DB >> 28599575 |
Bi-Cheng Fu1,2, Ji-Lu Lang1,2, Dong-Yang Zhang1,2, Lu Sun1,2, Wei Chen1,2, Wei Liu2, Kai-Yu Liu1,2, Chong-Yi Ma1,2, Shu-Lin Jiang1,2, Ren-Ke Li3,4, Hai Tian1,2.
Abstract
MicroRNA-34a (miR-34a) is expressed in the myocardium and expression is altered after myocardial injury. We investigated the effects of miR-34a on heart function after ischemia-reperfusion (IR) injury. Cardiomyocytes were isolated from neonatal rat hearts and simulated IR injury was induced in vitro. Following IR injury in rats, infarct size was measured and left ventricular (LV) function was evaluated using echocardiography. Protein expression of silent information regulator 1 (SIRT1), acetylated p53 (ac-p53), Bcl-2 and Bax, and miR-34a and SIRT1 gene levels were analyzed. miR-34a overexpression exacerbated myocardial injury by increasing apoptosis and infarct size and decreasing LV function. Suppression of miR-34a attenuated myocardial IR injury. SIRT1 was negatively regulated by miR-34a and the expression of downstream genes, such as ac-p53, Bcl-2, and Bax were altered correspondingly. Increased expression of miR-34a aggravates injury after IR; miR-34a suppression therapy may represent a new line of treatment for myocardial IR injury.Entities:
Keywords: SIRT1; apoptosis; cardiomyocytes; ischemia–reperfusion injury; microRNA-34a
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Year: 2017 PMID: 28599575 DOI: 10.1089/scd.2017.0062
Source DB: PubMed Journal: Stem Cells Dev ISSN: 1547-3287 Impact factor: 3.272