文章摘要
王健 全瑛 吉健华 王医林 赵花妮.TGF-beta1通过抑制HIF-1alpha减少风湿性心脏病心肌细胞胶原合成[J].,2014,14(34):6634-6636
TGF-beta1通过抑制HIF-1alpha减少风湿性心脏病心肌细胞胶原合成
Transforming Growth Factor beta 1 Inhibits the Collagen Synthesis ofRheumatic Cardiomyocytes by Reducing Hypoxia Inducible Factor -1 alpha
  
DOI:
中文关键词: 转化生长因子beta1  缺氧诱导因子-1alpha  风湿性心脏病心肌细胞  I型胶原
英文关键词: TGF-beta1  HIF-1alpha  Rheumatic cardiomyocytes  Type I collagen
基金项目:陕西省科学技术研究发展计划项目(2013K12-03-22)
作者单位
王健 全瑛 吉健华 王医林 赵花妮 西安市第五医院风湿科 
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中文摘要:
      目的:探讨缺氧诱导因子-1alpha(HIF-1alpha)在转化生长因子beta1(TGF-beta1)促风湿性心脏病心肌细胞胶原合成中的作用。方法:以体外培养风湿性心脏病(风心病)患者经瓣膜置换术后留取组织分离而来的心肌细胞为研究对象,依据加入TGF-beta1 的浓度将前 期实验分为四组:0,5,10 及20 (ug/L),观察TGF-beta1 对风湿性心脏病心肌细胞胶原合成及HIF-1alpha表达的影响;而后实验选取10 ug/L TGF-beta1 为干预浓度,将Scrambled siRNA 或HIF-1-alpha siRNA 转染入细胞内。48 小时后,分别收集各组细胞,采用RT-PCR检测I型胶原的mRNA 水平,Western Blot 技术测定细胞内I 型胶原和HIF-1琢的蛋白表达水平。结果:与0、5 及10 ug/L浓度 TGF-beta1 组相比,5、10 及20 ug/L浓度的TGF-beta1 分别显著地增加了风心病心肌细胞I型胶原及HIF-1-alpha的表达。另外,HIF-1alpha siRNA则明显减少了TGF-beta1 诱导的心肌细胞I型胶原生成。结论:HIF-1-alpha介导了TGF-beta1 对风湿性心脏病心肌细胞I型胶原合成的促进作用。
英文摘要:
      Objective:To elucidate the effect of hypoxia inducible factor -1 alpha(HIF-1alpha)on generation of Type I collagen in rheumatic cardiomyocytes induced by transforming growth factor beta 1 (TGF-beta1).Methods:Human rheumatic cardiomyocytes were cultured in vitro, the pre-experiment was divided into 4 groups as follows: 0, 5, 10 and 20 (ug/L), according to the concentration of TGF-beta1. Then, we chose 10 ug/L TGF-beta1, and transfected rheumatic cardiomyocytes with non-specific siRNA or HIF-1alpha siRNA. 48 hours later, the cells were collected. Type I collagen mRNA was detected by RT-PCR, the expression of Type I collagen and HIF-1alpha was determined by Western Blot.Results:Compared with 0, 5, 10 ug/L TGF-beta 1 groups, 5, 10, 20 ug/L TGF-beta1 significantly increased the synthesis of Type I collagen and expression of HIF-1alpha. In addition, HIF-1alpha siRNA markedly decreased generation of Type I collagen induced by TGF-beta 1.Conclusion:HIF-1alpha participates in TGF-beta1 induced synthesis of Type I collagen in rheumatic cardiomyocytes.
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