Oncotarget

Research Papers: Pathology:

MiR-499-5p protects cardiomyocytes against ischaemic injury via anti-apoptosis by targeting PDCD4

Yingqing Li _, Jianhua Lu, Xueming Bao, Xifu Wang, Junhua Wu, Xiongbin Li and Weiqiang Hong

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Oncotarget. 2016; 7:35607-35617. https://doi.org/10.18632/oncotarget.9597

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Abstract

Yingqing Li1,*, Jianhua Lu1,*, Xueming Bao1, Xifu Wang1, Junhua Wu1, Xiongbin Li1, and Weiqiang Hong1

1 Department of Emergency, Guangzhou First People’s Hospital, Guangzhou Medical University, Guangzhou, People’s Republic of China

* These authors have contributed equally to this article

Correspondence to:

Yingqing Li, email:

Keywords: miR-499-5p; acute myocardial infarction; cardiomyocytes apoptosis; ischaemic injury; programmed cell death 4; Pathology Section

Received: March 03, 2016 Accepted: May 17, 2016 Published: May 25, 2016

Abstract

Recent studies have reported that miRNAs might play critical roles in acute myocardial infarction (AMI). The objective of this study is to investigate the role of miR-499-5p in AMI and its potential molecular mechanisms. The expression level of MiR-499-5p was remarkably decreased in the infarcted myocardial tissues and in the cultured neonatal rat cardiomyocytes induced by hypoxia. Overexpression or knockdown of miR-499-5p decreased or increased the apoptotic rates of cultured cardiomyocytes in vitro. In addition, ectopic overexpression of miR-499-5p in the rat AMI models with agomir reduced the myocardial infarct size through decreasing the cardiomyocytes apoptosis in the infarcted area of the rat hearts. PDCD4 (programmed cell death 4) was verified as a direct target of miR-499-5p by luciferase report assay, and ectopic overexpression or inhibition of miR-499-5p could inhibit or increase the PDCD4 expression at both the mRNA and protein levels. Furthermore, we found that ectopic overexpression of PDCD4 without miR-499-5p binding sites reversed miR-499-5p-mediated cardiomyocytes apoptosis. Together, these findings revealed the role of miR-499-5p in protecting the cardiomyocytes against apoptosis induced by AMI via its direct target PDCD4, which providing evidence for the miR-499-5p/PDCD4 pathway as a potential therapeutic target for patients with AMI.


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