转化生长因子对心肌细胞胶原合成的影响  被引量:2

The Effect of Transforming Growth Factor Beta-1 on Collagen Synthesis of Cardiomyocytes in Rheumatic Heart Disease

在线阅读下载全文

作  者:宋智钢[1] 刘维永[2] 蔡振杰[2] 俞世强[2] 张近宝[2] 胡巧霞[2] 

机构地区:[1]第二军医大学附属长海医院胸心外科,上海210433 [2]第四军医大学西京医院心外科,陕西西安710032

出  处:《中国体外循环杂志》2003年第1期16-18,12,共4页Chinese Journal of Extracorporeal Circulation

基  金:国家自然科学基金资助项目 (3 9870 790 )

摘  要:目的 探讨转化生长因子 β1(TGF- β1)对风湿性心脏病 (风心病 )心肌细胞胶原合成的作用。方法 利用成熟心肌细胞体外培养模型 ,用反转录 -聚合酶链反应和 Western蛋白印迹方法检测 2 0 ng/ m l人 TGF- β1刺激后不同时间点 ,以及不同浓度人 TGF- β1(5、10、2 0 ng/ m l)刺激对正常人和风心病患者心肌细胞 、 型前胶原 m R-NA和 型胶原蛋白表达的影响。结果 人 TGF- β1对正常人心肌细胞胶原合成无刺激作用 ,但可促进风心病患者心肌细胞 、 型前胶原 m RNA和 型胶原蛋白的表达 ,且上调作用与刺激时间和浓度均呈依赖关系。结论  TGF- β1是风心病心肌细胞合成分泌胶原的重要刺激因子 。OBJECTIVE To investigate the effect of transforming growth factor beta 1 (TGF β1) on collagen synthesis in rheumatic cardiomyocytes. METHODS The adult cardiomyocytes of normal human or patients with rheumatic heart disease were cultured in vitro. The cardiomyocytes were stimulated by treating with human TGF β1. The expression of typeⅠ/Ⅲ procollagen mRNA and typeⅠcollagen in cardiomyocytes were observed by RT PCR and Western Blotting after stimulating with different concentration of human TGF β1 (5, 10, 20 ng · ml 1) and at different times after 20 ng · ml 1 human TGF β1 stimulation. RESULTS The treatment with human TGF β1 was able to activate cardiomyoctyes of patients with rheumatic heart disease to express typeⅠ/Ⅲ procollagen mRNA and typeⅠcollagen, and the actions depended on Stimulative dose or times, but it had no effect on normal cardiomyocytes. CONCLUSIONS TGF β1 is the important factor which activate rheumatic cardiomyocytes to synthesize and secrete collagen. It plays a key role in the phenotype transformation of cardiomyocytes and the myocardium fibrosis in rheumatic heart disease.

关 键 词:风湿性心脏病 转化生长因子Β1 心肌细胞 胶原 

分 类 号:R654.2[医药卫生—外科学] R451[医药卫生—临床医学]

 

参考文献:

正在载入数据...

 

二级参考文献:

正在载入数据...

 

耦合文献:

正在载入数据...

 

引证文献:

正在载入数据...

 

二级引证文献:

正在载入数据...

 

同被引文献:

正在载入数据...

 

相关期刊文献:

正在载入数据...

相关的主题
相关的作者对象
相关的机构对象