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J Appl Physiol 92: 2162-2168, 2002. First published January 4, 2002; doi:10.1152/japplphysiol.01192.2001
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Vol. 92, Issue 5, 2162-2168, May 2002

Effects of all-trans retinoic acid on angiotensin II-induced myocyte hypertrophy

Hao-Jie Wang, Yi-Chun Zhu, and Tai Yao

Kidney and Hypertension Research Center, Department of Physiology, Medical Center of Fudan University, Shanghai 200032, People's Republic of China

We used cultured neonatal rat cardiac myocytes to test the hypothesis that all-trans retinoic acid (atRA) may act to modulate ANG II actions in inducing myocyte hypertrophy. Our observations were as follows. 1) atRA (10-7 to ~10-5 M ) inhibited ANG II-induced hyperplasia of fibroblasts in a dose-dependent manner. 2) Treatment of atRA attenuated the ANG II-induced increase in total cell protein content. 3) Treated with ANG II (10-7 M) for 5 days, the cultured neonatal rat cardiac myocytes demonstrated an apparent accumulation of sarcomeric fiber proteins and Golgi's complex, as well as reorganization of the sarcomeric unit within individual myocytes. atRA (10-6 M) treatment reduced the accumulation of contractile proteins and Golgi's complex without affecting the ANG II-induced reorganization of the sarcomeric unit. 4) atRA attenuated the ANG II-induced increase in intracellular Ca2+. Our results show that atRA inhibits some effects of ANG II on neonatal rat cardiac myocytes and suggest that atRA may be a therapeutic candidate for the prevention and therapy of cardiac hypertrophy and remodeling.

cardiac hypertrophy; dedifferentiation; intracellular calcium; hyperplasia, induction of myocyte differentiation


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