The depressive effects of sTβRII on Smad signal induced by TGF-β1 in neonatal rat cardiac fibroblasts and myofibroblast differentiation

Objective To investigate the inhibitory effects of sTβRⅡ on Smad signal induced by TGF-β1 in neonatal rat cardiac fibroblasts and myofibroblast differentiation. Methods Cardiac fibroblasts obtained from neonatal rats were cultured and randomly divided into 4 groups: PBS control group,TGF-β1 (5 ng/ml) group,sTβRⅡ (50 ng/ml) group and TGF-β1+sTβRⅡ group. 30min,1h and 2h after the treatment,the expression of P-Smad2 and Smad3 was measured by immunocytochemistry (ICC) staining; after 24h,the expression of α-SMA was measured by ICC staining. Results Compared with that of PBS control group,the expression of P-Smad2,Smad3 (percentage of nuclear stained cells) and α-SMA increased significantly in TGF-β1 group (P0.05); compared with that of TGF-β1 group,the expression of P-Smad2,Smad3 (percentage of nuclear stained cells) and α-SMA decreased markedly in TGF-β1+sTβRⅡ group (P0.05). Conclusions sT Rβ Ⅱ antagonizes the phosphorylation and nuclear translocation of Smad2/Smad3 protein induced by TGF-β1,blocks Smad signal transduction pathway,and inhibits myofibroblast differentiation in neonatal rat cardiac fibroblasts.