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

• 实验研究 • 上一篇    下一篇

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. 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.   

  1. 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:

    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

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