Summary
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.
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Shuwang GE and Rui Zeng contributed equally to this work.
This project was supported by grants from National Natural Sciences Foundation of China (No. 30370657, No.30871172), and New Century Excellent Talents Grant (No. NCET004-0712).
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Ge, S., Zeng, R., Luo, Y. et al. Role of protein kinase C in advanced glycation end products-induced epithelial-mesenchymal transition in renal proximal tubular epithelial cells. J. Huazhong Univ. Sci. Technol. [Med. Sci.] 29, 281–285 (2009). https://doi.org/10.1007/s11596-009-0303-1
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DOI: https://doi.org/10.1007/s11596-009-0303-1