Role of Protein Kinase C in Advanced Glycation End Products-induced Epithelial-Mesenchymal Transition in Renal Proximal Tubular Epithelial Cells  被引量:2

Role of Protein Kinase C in Advanced Glycation End Products-induced Epithelial-Mesenchymal Transition in Renal Proximal Tubular Epithelial Cells

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作  者:葛树旺 曾锐 罗昀 刘琳 位红兰 张娟 周欢 徐钢 

机构地区:[1]Department of Nephrology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology

出  处:《Journal of Huazhong University of Science and Technology(Medical Sciences)》2009年第3期281-285,共5页华中科技大学学报(医学英德文版)

基  金:supported by grants from National Natural Sciences Foundation of China (No. 30370657, No.30871172);New Century Excellent Talents Grant (No. NCET004–0712)

摘  要:The role of protein kinase C (PKC) activation in advanced glycation end products (AGEs)-induced epithelial-mesenchymal transition in renal proximal tubular epithelial cells was investigated. HKC cells were divided into three groups: normal group, AGE-BSA group (100 mg/L AGE-BSA) and AGE-BSA+PKC inhibitor (10 μmol/L chelerythrine chloride) group. PKC activity was measured by PKC assay kit. The expression of Vimentin, and phosphorylated β-catenin was detected by using Western blotting, and the content of TGF-β1 was examined by ELISA method. The intracellular disposition of Vimentin was observed by fluorescence microscopy. As compared with normal group, PKC activity was increased significantly in AGE-BSA group. The expression of Vimentin, phosphorylated β-catenin, and TGF-β1 was enhanced significantly in AGE-BSA group. The expression of Vimentin, phosphorylated β-catenin, and TGF-β1 was significantly blocked by chelerythrine chloride. High expression of Vimentin, phosphorylated β-catenin, and TGF-β1 induced by AGE-BSA may be mediated via the activation of PKC signal transduction pathway.The role of protein kinase C (PKC) activation in advanced glycation end products (AGEs)-induced epithelial-mesenchymal transition in renal proximal tubular epithelial cells was investigated. HKC cells were divided into three groups: normal group, AGE-BSA group (100 mg/L AGE-BSA) and AGE-BSA+PKC inhibitor (10 μmol/L chelerythrine chloride) group. PKC activity was measured by PKC assay kit. The expression of Vimentin, and phosphorylated β-catenin was detected by using Western blotting, and the content of TGF-β1 was examined by ELISA method. The intracellular disposition of Vimentin was observed by fluorescence microscopy. As compared with normal group, PKC activity was increased significantly in AGE-BSA group. The expression of Vimentin, phosphorylated β-catenin, and TGF-β1 was enhanced significantly in AGE-BSA group. The expression of Vimentin, phosphorylated β-catenin, and TGF-β1 was significantly blocked by chelerythrine chloride. High expression of Vimentin, phosphorylated β-catenin, and TGF-β1 induced by AGE-BSA may be mediated via the activation of PKC signal transduction pathway.

关 键 词:protein kinase C advanced glycation end products epithelial-mesenchymal transition 

分 类 号:R692[医药卫生—泌尿科学]

 

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