Insulin prevents bone ic protein-4 induced cardiomyocyte apoptosis through activating Akt.pdf.pdf

Biochemical and Biophysical munications 456 (2015) 605–609
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Biochemical and Biophysical munications
journal homepage: ate/ybbrc
Insulin prevents bone ic protein-4 induced cardiomyocyte
apoptosis through activating Akt
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Yue Xing 1, Di Yang 1, Jing Lu, De-Li Dong
Department of Pharmacology (The State-Province Key Laboratories of Biomedicine-Pharmaceutics of China, Key Laboratory of Cardiovascular Research, Ministry of Education),
Harbin Medical University, Harbin 150086, PR China
article info abstract
Article history: Bone ic protein-4 (BMP4) mediates pathological cardiac hypertrophy. Insulin is well-known
Received 23 November 2014 to promote cardiomyocyte survival in heart diseases. The aim of the present study is to evaluate the
Available online 6 December 2014 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 mea-
Keywords: sured by using western blot technique. Insulin did not elicit cardiomyocyte apoptosis, but antagonized
Bone ic protein BMP4-induced cardiomyocyte apoptosis. Insulin treatment rapidly activated Akt which was inhibited
Insulin
by Akt inhibitor in cardiomyocytes. Furthermore, Akt inhibitor canceled the anti-apoptotic effects of
Cardiomyocyte
in