Journal
CURRENT PHARMACEUTICAL DESIGN
Volume 19, Issue 27, Pages 4865-4873Publisher
BENTHAM SCIENCE PUBL LTD
DOI: 10.2174/13816128113199990325
Keywords
Myocardial infarction; apoptosis; cardiomyocyte; MiRNA-34a; ALDH2; hypoxia
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Funding
- National Basic Research Program of China [2011CB503905]
- National Science Fund for Distinguished Young Scholars [30725036]
- National Natural Science Foundation of China [30971250]
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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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