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Am J Physiol Heart Circ Physiol 275: H2036-H2040, 1998;
0363-6135/98 $5.00
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Vol. 275, Issue 6, H2036-H2040, December 1998

Essential roles for G1 cyclin-dependent kinase activity in development of cardiomyocyte hypertrophy

Mimi Tamamori1, Hiroshi Ito1, Michiaki Hiroe1, Yoshio Terada1, Fumiaki Marumo1, and Masa-Aki Ikeda2

1 Second Department of Internal Medicine and 2 Department of Developmental Biology, Graduate School of Dentistry, Tokyo Medical and Dental University, Tokyo 113, Japan

Although cardiomyocytes undergo terminal differentiation soon after birth, irreversibly withdrawing from the cell cycle, growth stimulation induces cell hypertrophy. Such growth stimulation is also responsible for the upregulation of G1 cyclins and cyclin-dependent kinase (CDK) activity in proliferating cells. We sought to determine whether G1 CDK activity is involved in the hypertrophy of rat neonatal cardiomyocytes in culture. We show that serum stimulation promoted the G1 CDK activity without induction of DNA synthesis in cardiomyocytes. Furthermore, overexpression of CDK inhibitors p16INK4a and p21CIP1/WAF1 by use of the adenovirus vector effectively prevented cell enlargement and depressed serum-induced protein synthesis and expression of skeletal alpha -actin and atrial natriuretic factor, genetic markers of cardiac hypertrophy. These results suggest that the G1 CDK activity promoted by serum stimulation is required for the induction of cardiomyocyte hypertrophy and provide novel evidence for understanding the regulation of cardiac hypertrophy by cell cycle regulators.

terminal differentiation; cell cycle regulators


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