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《Chongqing Medicine》 2011-09
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Role of ERK1/2 signaling pathway on angiotensin-(1-7) inhibit rat′s tubular epithelial myofibroblast transdifferentiation induced by angiotensinⅡ

Wang Mingyong1,Yuan Bo2,Xia Jiyi1,Chen Feng1,Chen Zhuang1,Liu Jian3(1.Medical Experimental Center,Affiliated Hospital,Luzhou Medical College,Luzhou,Sichuan 646000,China;2.Yibin First Pople′s Hospital,Yibin,Sichuan 644000 China;3.Departmen of Nephrology,Affiliated Hospital,Luzhou Medical College,Luzhou,Sichuan 646000,China)  
Objective To explore the role of ERK1/2 signaling pathway on angiotensin-(1-7) inhibit rat′s tubular epithelial myofibroblast transdifferentiation induced by angiotensinⅡ.Methods NRK52E were maintained and sub-cultured.The NRK52E cells were stimulated by angiotensin-(1-7) and angiotensinⅡ(both 10-6 mol/L),cultured for 24,48,72,96 h,we detected the expressions of E-cadherin and α-SMA by immunocytochemistry method;cultured for 72,96 h,ERK1/2,detected by Western blot.Results The cells,cultured for 96h,expressions of α-SMA and P-ERK1/2 of AngⅡ group increased significantly than that of control group(P0.05),expressions of E-cadherin of AngⅡ group decreased significantly than that of control group(P0.05);expressions of α-SMA and P-ERK1/2 of AngⅡ+Ang-(1-7) group decreased significantly than that of AngⅡ group at the same time(P0.05),expressions of E-cadherin of AngⅡ+Ang-(1-7) group increased than that of AngⅡ group at the same time(P0.05).Conclusion Ang-(1-7) can inhibit AngⅡ-induced tubular epithelial myofibroblast transdifferentiation.ERK1/2 signaling pathway plays an important role in rat′s tubular epithelial myofibroblast transdifferentiation.
【Fund】: 国家自然科学基金资助项目(30771008)
【CateGory Index】: R692
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