Angiopoietin-1 protects H9c2 cells from H2O2-induced apoptosis through AKT signaling

Abstract

Loss of cardiomyocytes by apoptosis is proposed to cause ventricular remodeling and heart failure. Reactive oxygen species-induced apoptosis of cardiomyocytes has been reported to play an important role in many types of pathological processes of the heart. We investigated whether angiopoietin-1 (Ang1) has direct cytoprotective effects on cardiomyocytes against oxidative stress. Cultured H9c2 cells (cardiomyocytes) were treated with hydrogen peroxide (H(2)O(2)). Apoptosis was evaluated by flow cytometry, TUNEL assay and DNA laddering. The H(2)O(2) treatment caused typical apoptosis of H9c2 cells in a time-dependent manner. Transfection of recombinant adenovirus expressing Ang1 resulted in a sustained phosphorylation of AKT and inhibition of H(2)O(2)-induced apoptosis in H9c2 cells. This effect could be reversed by AKT inhibition. These results suggest that Ang1 protects cardiomyocytes from oxidative stress-induced apoptosis by regulating the activity of AKT.