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Aim:To determine whether all-trans retinoic acid(atRA)acts to modulate angio-tensin 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 wasused to detect cell growth of the CF;and immunocytochemistry and Westernblotting were used to measure the production and secretion of collagen and theexpression of transforming growth factor-β_1(TGF-β_1)by the CF.Results:atRA(1×10~(-7) to 1×10~(-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(1×10~(-6) mol/L),butnot by AT_2 receptor antagonist PD 123319 (up to 1×10~(-6) mol/L).Exposure of CF toatRA(1×10~(-5) mol/L)attenuated the Ang Ⅱ-induced increase in the secretion ofcollagen types Ⅰ and Ⅲ(P<0.05).atRA (1×10~(-5) mol/L)also blocked the Ang Ⅱ-induced increase in the expression of TGF-β_1.Conclusion:atRA inhibits the AngⅡ-induced increase in cell growth and collagen secretion of neonatal rat CF.Theeffect of atRA is possibly mediated by lowering the TGF-β_1 level.These observa-tions support the notion that atRA is a potential candidate for the prevention andtherapy of cardiac remodeling.
Aim: To determine whether all-trans retinoic acid (atRA) acts to modulate angio-tensin 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 theexpression of transforming growth factor-β_1 (TGF-β_1) by the CF. Results: atRA (1 × 10 -7 to 1 × 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 (1 × 10 -6 mol / L), butnot by AT_2 receptor antagonist PD 123319 (up to 1 × 10 -6 mol / L) .Exposure of CF toatRA (1 × 10 -5 mol / L) attenuated the Ang Ⅱ-induced increase in the secretion ofcollagen types Ⅰ and Ⅲ (P <0.05) .a tRA (1 × 10 ~ (-5) mol / L) also blocked the Ang Ⅱ-induced increase in the expression of TGF-β_1.Conclusion: atRA inhibits the AngⅡ-induced increase in cell growth and collagen secretion of neonatal rat CF. Theeffect of atRA is possibly mediated by lowering the TGF-β_1 level. The observa-tions support the not that that atRA is a potential candidate for the prevention and treatment of cardiac remodeling.