广东医学2017，Vol.38Issue(14)：2109-2113,5.
草酸钙晶体引起肾小管上皮细胞紧密连接损伤与TRPV5变化的调节机制
The regulatory mechanism of CaOx crystal-induced TJs injury and TRPV5 in renal tubular epithelial cells
摘要
Abstract
Objective To investigate the regulatory mechanism of CaOx crystal induced tight junctions(TJs) injury and TRPV5 in renal tubular epithelial cells.Methods Calcium oxalate monohydrate (COM) exposure was performed on canine renal tubular epithelial cells (MDCK) and HEK-293 cells with stable over-expression of TRPV5.EGTA was administrated for TJs injury model.Western blot, immunofluorescence, polarizing microscope and other indicators were applied to assess TJs protein, Na+-K+-ATPase, TRPV5 and crystal adhesion etc.Results COM significantly down-regulated Occludin and ZO-1 protein expression in MDCK cells (P<0.01).The TJs injury significantly increased the adhesion ability of COM to MDCK cells (P<0.05).The expression of Na+-K+-ATPase induced TJs recovery and reached the highest level at 1min.COM inhibited the expression of TRPV5 membrane protein and total protein in HEK-293 cells (P<0.01).Conclusion CaOx can induce the TJs injury in renal tubular epithelial cells, and promote the adhesion of CaOx crystals.When the cell olarity is destroyed, the TRPV5 membrane protein gets transportation problem and thus the expression of TRPV5 membrane protein ecreases.With the increase of urinary calcium, the negative feedback from Na+-K+-ATPase stimulates the repairmen of TJs.With the self-repairmen of TJs, CaOx crystal adhesion to cells decreases.关键词
草酸钙晶体/肾小管上皮/紧密连接/TRPV5Key words
calcium oxalate crystal/renal tubular epithelial/tight junction/crystal adhesion/TRPV5引用本文复制引用
卢穗琳,钟文,李淑珏,赵志健..草酸钙晶体引起肾小管上皮细胞紧密连接损伤与TRPV5变化的调节机制[J].广东医学,2017,38(14):2109-2113,5.基金项目
广东省优秀青年教师培养计划项目(编号:B158027),广州市科技计划项目(编号:201610010169),广州市市属高校科研项目(编号:1201620038) （编号:B158027）
