Insulin prevents bone morphogenetic protein-4 induced cardiomyocyte apoptosis through activating Akt.
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.
['Xing|Yue|Y|', 'Yang|Di|D|', 'Lu|Jing|J|', 'Dong|De-Li|DL|']
D000818:Animals D017209:Apoptosis D055415:Bone Morphogenetic Protein 4 D002478:Cells, Cultured D004789:Enzyme Activation D007328:Insulin D032383:Myocytes, Cardiac D051057:Proto-Oncogene Proteins c-akt D051381:Rats
Insulin Cardiomyocyte Apoptosis Bone morphogenetic protein