MicroRNA-34a Promotes Cardiomyocyte Apoptosis Post Myocardial Infarction Through Down-regulating Aldehyde Dehydrogenase 2

Author(s): Fan Fan, Aijun Sun, Hangtian Zhao, Xiangwei Liu, Wenbin Zhang, Xueting Jin, Cong Wang, Xin Ma, Cheng Shen, Yunzeng Zou, Kai Hu, Junbo Ge.

Journal Name: Current Pharmaceutical Design

Volume 19 , Issue 27 , 2013

Submit Manuscript
Submit Proposal

Abstract:

MicroRNA-34a (miR-34a) promotes apoptosis via down-regulating many anti-apoptotic proteins. Aldehyde dehydrogenase 2 (ALDH2) is an anti-apoptotic enzyme whose activity decline associates with myocardial injury. We tested hypothesis that miR-34a might play a pro-apoptotic role in myocardial infarction (MI) by down-regulating ALDH2. MiR-34a was highly increased while ALDH2 expression was decreased after experimental MI. Overexpression of miR-34a in neonatal rat cardiomyocyte could significantly enhance apoptosis and down-regulate ALDH2 expression. In 293 cells, luciferase reporter assay results demonstrated that ALDH2 was a direct target of miR-34a. Serum miR-34a levels in acute myocardial infarction (AMI) patients and rats were significantly higher than healthy subjects and sham rats. Our results proved that miR-34a could promote cardiomyocyte apoptosis via negatively regulating ALDH2 and circulating miR-34a was increased in the condition of MI. Thus, miR-34a may constitute a new therapeutic target and diagnostic marker for patients with MI.

Keywords: Myocardial infarction, apoptosis, cardiomyocyte, MiRNA-34a, ALDH2, hypoxia.

Rights & PermissionsPrintExport Cite as


Article Details

VOLUME: 19
ISSUE: 27
Year: 2013
Page: [4865 - 4873]
Pages: 9
DOI: 10.2174/13816128113199990325

Article Metrics

PDF: 67