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学科主题: 临床医学
题名:
Over-expressing transient receptor potential cation channel 6 in podocytes induces cytoskeleton rearrangement through increases of intracellular Ca2+ and RhoA activation
作者: Jiang, Lina1; Ding, Jie1; Tsai, Haojan2; Li, Lin2; Feng, Quancheng1; Miao, Jing1; Fan, Qingfeng1
关键词: podocyte ; over-expressing TRPC6 ; RhoA pathway ; cytoskeleton rearrangement
刊名: EXPERIMENTAL BIOLOGY AND MEDICINE
发表日期: 2011-02-01
DOI: 10.1258/ebm.2010.010237
卷: 236, 期:2, 页:184-193
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Medicine, Research & Experimental
研究领域[WOS]: Research & Experimental Medicine
关键词[WOS]: FOCAL SEGMENTAL GLOMERULOSCLEROSIS ; SLIT DIAPHRAGM ; GLOMERULAR-DISEASES ; ACTIN CYTOSKELETON ; VASCULAR MYOCYTES ; HUMAN TRPC6 ; CELLS ; DIACYLGLYCEROL ; ORGANIZATION ; GTPASES
英文摘要:

Transient receptor potential cation channel 6 (TRPC6) is one of the key molecules for filtration barrier function of podocytes. Over-expression of TRPC6 in podocytes is frequently found in acquired or inherited proteinuric kidney diseases, and animal model over-expression of TRPC6 may lead to proteinuria. To investigate the impact of TRPC6 over-expression in podocytes on its function and its relation to proteinuria in kidney diseases, we over-expressed TRPC6 in mouse podocytes by transient transfection of TRPC6 cDNA plasmid, and observed their changes in foot processes, intracellular F-actin distribution, nephrin and synaptopodin expression, electrophysiology, RhoA activity and intracellular Ca2+. In podocytes over-expressing TRPC6, cell processes were reduced remarkably in association with the derangement of cytoskeleton demonstrated by the abnormal distribution of intracellular F-actin. These cells also displayed a higher increase of intracellular Ca2+ ion to the TRPC6 agonist 1-oleoyl-acetyl-sn-glycerol and a higher current in the patch-clamp experiment, down-regulation of nephrin and synaptopodin expression and increase of activated RhoA. These changes could be rescued by the treatment of the cells with U73122 to block TRPC6 channel or BAPTA-AM to chelate intracellular Ca2+ ion. Additionally, the podocytes over-expressing TRPC6 treated with RhoA inhibitor Y-27632 showed an improvement in F-actin arrangement in the cells and increase of nephrin and synaptopodin expression. From these results, we therefore propose that over-expression of TRPC6 in podocytes may be one of the fundamental changes relating to the dysfunction of the slit diaphragm and proteinuria. Podocytes over-expressing TRPC6 may lead to higher intracellular Ca2+ ion concentration in the presence of stimuli. The increase of intracellular Ca2+ down-regulates the expression of two important molecules, nephrin on slit diaphragm and synaptopodin in cytoskeleton, and stimulates RhoA activity, which in turn causes F-actin derangement and the decrease of foot processes.

语种: 英语
所属项目编号: 30830105 ; 30801250 ; 7072080
项目资助者: National Nature Science Foundation of China ; Nature Science Foundation of Beijing
WOS记录号: WOS:000290122600009
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/63706
Appears in Collections:北京大学第一临床医学院_儿科_期刊论文

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作者单位: 1.Peking Univ, Hosp 1, Cent Lab, Beijing 100034, Peoples R China
2.Peking Univ, Hosp 1, Dept Pediat, Beijing 100034, Peoples R China

Recommended Citation:
Jiang, Lina,Ding, Jie,Tsai, Haojan,et al. Over-expressing transient receptor potential cation channel 6 in podocytes induces cytoskeleton rearrangement through increases of intracellular Ca2+ and RhoA activation[J]. EXPERIMENTAL BIOLOGY AND MEDICINE,2011,236(2):184-193.
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