Insulin prevents bone morphogenetic protein-4 induced cardiomyocyte apoptosis through activating Akt

• BMP4 induces cardiomyocyte apoptosis.
• Insulin prevents BMP4-induced cardiomyocyte apoptosis.
• Activation of Akt contributes to the protective effects of insulin.

Bone morphogenetic protein-4 (BMP4) mediates pathological cardiac hypertrophy. Insulin is well-known to promote cardiomyocyte survival in heart diseases. The aim of the present study is to evaluate the effects of insulin on BMP4-induced cardiomyocyte apoptosis. Cell viability and apoptosis were measured by using MTT, live and dead staining, caspase-3 activity assays, and the protein expressions were measured by using western blot technique. Insulin did not elicit cardiomyocyte apoptosis, but antagonized BMP4-induced cardiomyocyte apoptosis. Insulin treatment rapidly activated Akt which was inhibited by Akt inhibitor in cardiomyocytes. Furthermore, Akt inhibitor canceled the anti-apoptotic effects of insulin against BMP4 in cardiomyocytes. In conclusion, insulin prevents BMP4-induced cardiomyocyte apoptosis and the underlying mechanisms include activation of Akt. The present work provides a novel mechanism of the protective effects of insulin in cardiovascular system.