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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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