sTβRⅡ拮抗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

中国临床解剖学杂志 ›› 2010, Vol. 28 ›› Issue (2): 184-.

sTβRⅡ拮抗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

廉瑞青¹，　陈跃杰²，　许增禄¹，　张晓东²

1. 中国医学科学院基础医学研究所北京协和医学院基础学院人体解剖与组织胚胎学系，北京 100005；
2. 清华大学医学院，北京 100084

收稿日期:2009-11-03 出版日期:2010-03-25 发布日期:2010-04-13
通讯作者: 张晓东，教授，博士生导师，Tel：(010) 62797970，E-mail：zhxd@tsinghua.edu.cn E-mail:lianruiqing2005@163.com
作者简介:廉瑞青(1980-)，女，汉族，河南焦作人，博士研究生，研究方向：心血管生物学
基金资助:
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 )

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

LIAN Rui-qing, CHEN Yue-jie, ZHANG Xiao-dong，et al.

Department of Anatomy, Histology and Embryology, Institute of Basic Medical Sciences, Chinese Academy of Medical Science, School of Basic Medicine, Peking Union Medical College, Beijing 100005, China

Received:2009-11-03 Online:2010-03-25 Published:2010-04-13

摘要/Abstract

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 (5 ng/ml)组、sTβRⅡ (50 ng/ml)组和TGF-β1+ sTβRⅡ组。30 min、1 h和2 h后，免疫细胞化学染色检测P-Smad2和Smad3的表达；24 h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。

关键词: sTβRⅡ, 心肌成纤维细胞, TGF-β1, 信号转导, 肌成纤维细胞分化

Abstract:

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 (P＜0.05); 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 (P＜0.05). Conclusions　sT RβⅡ 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.

Key words: sTβRⅡ, Cardiac Fibroblasts, TGF-β1, Signal transduction, Myofibroblast differentiation

中图分类号:

R542.2

廉瑞青, 陈跃杰, 许增禄, 张晓东. sTβRⅡ拮抗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[J]. 中国临床解剖学杂志, 2010, 28(2): 184-.

LIAN Rui-Jing, CHEN Ti-Jie, HU Ceng-Lu, ZHANG Xiao-Dong. The depressive effects of sTβRⅡ on Smad signal induced by TGF-β1 in neonatal rat cardiac fibroblasts and myofibroblast differentiation[J]. Chinese Journal Of Clinical Anatomy, 2010, 28(2): 184-.

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