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Biochem Biophys Res Commun. 2016 Sep 23;478(3):1165-72. doi: 10.1016/j.bbrc.2016.08.086. Epub 2016 Aug 17.

miR-22 regulates starvation-induced autophagy and apoptosis in cardiomyocytes by targeting p38α.

Author information

1
Department of Cardiology, Changhai Hospital, Second Military Medical University, Shanghai 200433, China.
2
Institution of Thoracic Cardiac Surgery, Department of Cardiothoracic Surgery, Changhai Hospital, Shanghai 200433, China.
3
Department of Cardiology, Changhai Hospital, Second Military Medical University, Shanghai 200433, China. Electronic address: mlp-125@163.com.
4
Department of Cardiology, Changhai Hospital, Second Military Medical University, Shanghai 200433, China. Electronic address: xianxianz2010@163.com.

Abstract

microRNAs (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.

KEYWORDS:

Apoptosis; Autophagy; Cardiomyocytes; Myocardial infarction; microRNAs; p38α

PMID:
27544030
DOI:
10.1016/j.bbrc.2016.08.086
[Indexed for MEDLINE]

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