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.
Current Pharmaceutical Design
Title:MicroRNA-34a Promotes Cardiomyocyte Apoptosis Post Myocardial Infarction Through Down-regulating Aldehyde Dehydrogenase 2
Volume: 19 Issue: 27
Author(s): Fan Fan, Aijun Sun, Hangtian Zhao, Xiangwei Liu, Wenbin Zhang, Xueting Jin, Cong Wang, Xin Ma, Cheng Shen, Yunzeng Zou, Kai Hu and Junbo Ge
Affiliation:
Keywords: Myocardial infarction, apoptosis, cardiomyocyte, MiRNA-34a, ALDH2, hypoxia.
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.
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Cite this article as:
Fan Fan, Sun Aijun, Zhao Hangtian, Liu Xiangwei, Zhang Wenbin, Jin Xueting, Wang Cong, Ma Xin, Shen Cheng, Zou Yunzeng, Hu Kai and Ge Junbo, MicroRNA-34a Promotes Cardiomyocyte Apoptosis Post Myocardial Infarction Through Down-regulating Aldehyde Dehydrogenase 2, Current Pharmaceutical Design 2013; 19 (27) . https://dx.doi.org/10.2174/13816128113199990325
DOI https://dx.doi.org/10.2174/13816128113199990325 |
Print ISSN 1381-6128 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-4286 |
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