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C3a Mediates Epithelial-to-Mesenchymal Transition in Proteinuric Nephropathy
Tang, Ziyong2,3; Lu, Bao4,5; Hatch, Ellen; Sacks, Steven H.2; Sheerin, Neil S.1
刊名JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY
2009-03-01
DOI10.1681/ASN.2008040434
20期:3页:593-603
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Urology & Nephrology
研究领域[WOS]Urology & Nephrology
关键词[WOS]EXPERIMENTAL NEPHROTIC SYNDROME ; MEMBRANE ATTACK COMPLEX ; ADRIAMYCIN NEPHROPATHY ; RENAL INJURY ; TUBULOINTERSTITIAL DAMAGE ; ALTERNATIVE PATHWAY ; LUPUS NEPHRITIS ; 2 PARTS ; CELLS ; PROGRESSION
英文摘要

Tubulointerstitial inflammation and progressive fibrosis are common pathways that lead to kidney failure in proteinuric nephropathies. Activation of the complement system has been implicated in the development of tubulointerstitial injury in clinical and animal studies, but the mechanism by which complement induces kidney injury is not fully understood. Here, we studied the effect of complement on the phenotype of tubular epithelial cells. Tubular epithelial cells exposed to serum proteins adopted phenotypic and functional characteristics of mesenchymal cells. Expression of E-cadherin protein decreased and expression of both or-smooth muscle actin protein and collagen I mRNA increased. Exposure of the cells to the complement anaphylotoxin C3a induced similar features. Treating with a C3a receptor (C3aR) antagonist prevented both C3a- and serum-induced epithelial-to-mesenchymal transition. In the adriamycin-induced proteinuria model, C3aR-deficient mice demonstrated less injury, preserved renal function, and improved survival compared with wild-type mice. Furthermore, the kidneys of C3aR-deficient mice had significantly less interstitial collagen I and cc-smooth muscle actin. In summary, the complement anaphylotoxin C3a is an important mediator of glomerular and tubulointerstitial injury and can induce tubular epithelial-to-mesenchymal transition.

语种英语
WOS记录号WOS:000264084300021
资助机构KC Wong Foundation
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被引频次:67[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/54747
专题北京大学第三临床医学院_肾内科
作者单位1.Newcastle Univ, Sch Clin Med Sci, Inst Celular Med, Newcastle Upon Tyne NE2 4HH, Tyne & Wear, England
2.Kings Coll London, Guys Hosp London, Dept Nephrol & Transplantat, London WC2R 2LS, England
3.Peking Univ, Hosp 3, Dept Nephrol, Beijing 100871, Peoples R China
4.Harvard Univ, Childrens Hosp, Sch Med, Div Pulm Med, Boston, MA 02115 USA
5.Harvard Univ, Childrens Hosp, Sch Med, Ina Sue Perlmutter Lab, Boston, MA 02115 USA
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Tang, Ziyong,Lu, Bao,Hatch, Ellen,et al. C3a Mediates Epithelial-to-Mesenchymal Transition in Proteinuric Nephropathy[J]. JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY,2009,20(3):593-603.
APA Tang, Ziyong,Lu, Bao,Hatch, Ellen,Sacks, Steven H.,&Sheerin, Neil S..(2009).C3a Mediates Epithelial-to-Mesenchymal Transition in Proteinuric Nephropathy.JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY,20(3),593-603.
MLA Tang, Ziyong,et al."C3a Mediates Epithelial-to-Mesenchymal Transition in Proteinuric Nephropathy".JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY 20.3(2009):593-603.
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