All-trans retinoic acid inhibited angiotensin II-induced increase in cell growth and collagen secretion of neonatal cardiac fibroblasts.

AIM: To determine whether all-trans retinoic acid (atRA) acts to modulate angiotensin II (Ang II)-induced cardiac fibroblast cell growth and collagen secretion.
METHODS: Cultured neonatal rat cardiac fibroblasts (CF) were used in the experiment. A 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay was used to detect cell growth of the CF; and immunocytochemistry and Western blotting were used to measure the production and secretion of collagen and the expression of transforming growth factor-beta1 (TGF-beta1) by the CF.
RESULTS: atRA (10(-7) to 10(-5) mol/L) inhibited the Ang II-induced increase in cell growth of CF (P<0.05). Ang II stimulated the secretion of collagen types I and III by the CF. This effect was blocked by AT(1) receptor antagonist losartan (10(-6) mol/L), but not by AT2 receptor antagonist PD123319 (up to 10(-6) mol/L). Exposure of CF to atRA (10(-5) mol/L) attenuated the Ang II-induced increase in the secretion of collagen types I and III (P<0.05). atRA (10(-5) mol/L) also blocked the Ang II-induced increase in the expression of TGF-beta1.
CONCLUSION: atRA inhibits the Ang II-induced increase in cell growth and collagen secretion of neonatal rat CF. The effect of atRA is possibly mediated by lowering the TGF-beta1 level. These observations support the notion that atRA is a potential candidate for the prevention and therapy of cardiac remodeling.