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標題: Hexavalent chromium induces expression of mesenchymal and stem cell markers in renal epithelial cells
作者: Li, Wei-Jen
Yang, Cheng-Lin
Chow, Kuan-Chih
Kuo, Ting-Wei
關鍵字: CD133;Cr(VI);DDH;EMT;connexin-43;nanog;paxillin;vimentin;AC133 Antigen;Actins;Antigens, CD;Ascorbic Acid;Biomarkers;Cell Line;Cell Proliferation;Chromium;Epithelial Cells;Epithelial-Mesenchymal Transition;Gene Expression Regulation;Glycoproteins;Homeodomain Proteins;Humans;Kidney;Mesenchymal Stromal Cells;Nanog Homeobox Protein;Oxidoreductases;Peptides;Vimentin
Project: Molecular carcinogenesis, Volume 55, Issue 2, Page(s) 182-92.
Cr(VI) causes severe kidney damage. The patient's renal function could gradually recover by spontaneous kidney regeneration. The molecular effect of Cr(VI) on recovery of kidney cells, however, has not been clearly elucidated. Here we show that Cr(VI) induces expression of mesenchymal and stem cell markers, cell markers, such as paxillin, vimentin, α-SMA, nanog, and CD133 of HK-2 cells. Moreover, Cr(VI) activates epithelial-to-mesenchymal transition (EMT). By revealing that levels of dihydrodiol dehydrogenase were promptly reduced following Cr(VI) challenge, our data suggested that DDH could be involved in a Cr(VI)-related oxidation to generate massive reactive oxygen species and H2 O2 , and to create intracellular hypoxia, which then increased levels of SUMO-1 activating enzyme subunit 2, and sumoylation of eukaryotic elongation factor-2, to mediate the subsequent molecular and cellular responses, e.g., expression of mesenchymal and stem cell markers. Pretreatment with vitamin C reduced Cr(VI)-related cellular effects. However, no evident effect was observed when vitamin C was added following Cr(VI) challenge.
DOI: 10.1002/mc.22268
Appears in Collections:生物醫學研究所

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