Guoran Li, Guokun Wang, Liangliang Ma, Jun Guo, Jingwen Song, Liping Ma, Xianxian Zhao
Biochemical and biophysical research communications 2016 Sep 23microRNAs (miRNAs) are short noncoding RNAs that function in RNA silencing and post-transcriptional regulation of gene expression. They play critical regulatory roles in many cardiovascular diseases, including ischemia-induced cardiac injury. Here, we report microRNA-22, highly expressed in the heart, can protect cardiomyocytes from starvation-induced injury through promoting autophagy and inhibiting apoptosis. Quantitative real-time PCR (qPCR) demonstrated that the expression of miR-22 in starvation-treated neonatal rat cardiomyocytes (NRCMs) was markedly down-regulated. Over-expression of miR-22 significantly promoted starvation-induced autophagy and inhibited starvation-induced apoptosis in NRCMs. In contrast, reduction of miR-22 suppressed autophagy and accelerated apoptosis in starving NRCMs. Immunohistochemistry and TUNEL staining results also provided further evidence that miR-22 promoted autophagy and inhibited apoptosis in myocardial cells. Furthermore, both luciferase reporter assay and western blot analysis were performed to identify p38α as a direct target of miR-22. Taken together, miR-22 plays an important role in regulating autophagy and apoptosis in ischemic myocardium through targeting p38α. miR-22 may represent a potential therapeutic target for the treatment of ischemic heart diseases. Copyright © 2016 Elsevier Inc. All rights reserved.
Guoran Li, Guokun Wang, Liangliang Ma, Jun Guo, Jingwen Song, Liping Ma, Xianxian Zhao. miR-22 regulates starvation-induced autophagy and apoptosis in cardiomyocytes by targeting p38α. Biochemical and biophysical research communications. 2016 Sep 23;478(3):1165-72
PMID: 27544030
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