尾加压素Ⅱ对心肌成纤维细胞表型转换的影响

Effects of Urotensin Ⅱ on Phenotypic Transition of Cardiac Fibroblasts

目的探讨尾加压素Ⅱ对心肌成纤维细胞表型转换的影响。方法培养1 d龄乳鼠心肌成纤维细胞,用酶联免疫吸附测定(enzyme-linked immunosorbent assay,ELISA)法检测细胞上清液中Ⅰ型胶原含量,免疫荧光法及免疫印迹法测定α-平滑肌肌动蛋白(α-smooth muscle actin,α-SMA)表达,免疫印迹法检测细胞外调节蛋白激酶(extracellularregulatedprotein kinases,ERK)磷酸化;并观察ERK通路阻断药PD98059对尾加压素Ⅱ促进心肌成纤维细胞表型转换的影响。结果尾加压素Ⅱ刺激后,心肌成纤维细胞上清液中Ⅰ型胶原含量显著提高,胞内α-SMA表达明显增高浓集、ERK磷酸化显著提高。给予PD98059后,α-SMA表达明显下调。结论尾加压素Ⅱ可以诱导体外培养的心肌成纤维细胞表型转换,机制与上调ERK通路有关。

Objective To observe effects of Urotensin Ⅱ（U Ⅱ） on phenotypic transition of cardiac fibroblasts. Methods In the primary culture of neonatal rat cardiac fibroblasts（CFs）,as indexes of phenotypic transition,type I collagen was assessed by ELISA,α-SMA expression were assessed by immunoblotting and immunocytochemistry;ERK phosphorylation was determined by immunoblotting.Moreover,we evaluated the effect of ERK inhibitor PD98059 on the promotion of U Ⅱ in CFs phenotypic transition. Results U Ⅱ can enhance the type I collagen level,α-SMA and ERK phosphorylation.After PD98059 treatment,α-SMA expression was obviously depressed. Conclusion Urotensin Ⅱ can induce phenotypic transition of cardiac fibroblasts,the mechanisms are associated with enhancing ERK phosphorylation.