MicroRNA ‑1 downregulation induced by carvedilol protects cardiomyocytes against apoptosis by targeting heat shock protein 60.

MicroRNA‑1 downregulation induced by carvedilol protects cardiomyocytes against apoptosis by targeting heat shock protein 60. Mol Med Rep. 2019 Mar 14;: Authors: Hu Y, Chen X, Li X, Li Z, Diao H, Liu L, Zhang J, Ju J, Wen L, Liu X, Pan Z, Xu C, Hai X, Zhang Y Abstract Myocardial infarction (MI) is the most common event in cardiovascular disease. Carvedilol, a β‑blocker with multiple pleiotropic actions, is widely used for the treatment cardiovascular diseases. However, the underlying mechanisms of carvedilol on alleviating MI are not fully understood. The aim of the present study was to investigate whether the beneficial effects of carvedilol were associated with regulation of microRNA‑1 (miR‑1). It was demonstrated that carvedilol ameliorated impaired cardiac function and decreased infarct size in a rat model of MI induced by coronary artery occlusion. Similarly, carvedilol reversed the H2O2‑induced decrease in cardiomyocyte viability in a dose‑dependent manner. The in vivo and in vitro models demonstrated the downregulation of miR‑1 following treatment with carvedilol. Overexpression of miR‑1, a known pro‑apoptotic miRNA, decreased cell viability and induced cell apoptosis. Transfection of miR‑1 abolished the beneficial effects of carvedilol. The expression of heat shock protein 60 (HSP60), a direct target of miR‑1, was identified to be decreased in MI and H2O2‑induced apoptosis, which was associated with...
Source: Molecular Medicine Reports - Category: Molecular Biology Tags: Mol Med Rep Source Type: research