摘要
目的研究可溶性转化生长因子-β1Ⅱ型受体(sTβRⅡ)对新生大鼠心肌成纤维细胞内TGF-β1诱导的Smad信号和肌成纤维细胞分化的抑制效应。方法培养新生大鼠的心肌成纤维细胞,随机分为4组:PBS对照组、TGF-β1(5ng/ml)组、sTβRⅡ(50ng/ml)组和TGF-β1+sTβRⅡ组。30min、1h和2h后,免疫细胞化学染色检测P-Smad2和Smad3的表达;24h后,免疫细胞化学染色检测α-SMA的表达。结果与PBS对照组相比,TGF-β1组P-Smad2、Smad3(核阳性率)和α-SMA的表达显著性升高(P<0.05);与TGF-β1组相比,TGF-β1+sTβRⅡ组P-Smad2、Smad3(核阳性率)和α-SMA的表达明显降低(P<0.05)。结论sTβRⅡ可拮抗新生大鼠心肌成纤维细胞内TGF-β1诱导的Smad2/Smad3蛋白的磷酸化与核转位,阻断Smad信号转导通路,抑制肌成纤维细胞分化。
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.
出处
《中国临床解剖学杂志》
CSCD
北大核心
2010年第2期184-187,共4页
Chinese Journal of Clinical Anatomy
基金
清华-裕元医学科学研究基金(20240000546)
清华大学伍舜德医学科学研究基金(20240000807)
