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

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.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Li G,Wang G,Ma L,Guo J,Song J,Ma L,Zhao X

doi

10.1016/j.bbrc.2016.08.086

subject

Has Abstract

pub_date

2016-09-23 00:00:00

pages

1165-72

issue

3

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(16)31343-2

journal_volume

478

pub_type

杂志文章

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