学科主题基础医学
Distinct Roles for Basal and Induced COX-2 in Podocyte Injury
Cheng, Huifang1,2; Fan, Xiaofeng1,2; Guan, Youfei5; Moeckel, Gilbert W.3; Zent, Roy1,2; Harris, Raymond C.1,2
刊名JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY
2009-09-01
DOI10.1681/ASN.2009010039
20期:9页:1953-1962
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]THROMBOXANE-SYNTHASE INHIBITION ; MURINE LUPUS NEPHRITIS ; CYCLOOXYGENASE-2 EXPRESSION ; CYCLOSPORINE NEPHROTOXICITY ; EPITHELIAL-CELLS ; RENAL INJURY ; RECEPTOR ANTAGONIST ; REMNANT KIDNEY ; DEFICIENT MICE ; DIABETIC-RATS
英文摘要

Transgenic mice that overexpress cyclooxygenase-2 (COX-2) selectively in podocytes are more susceptible to glomerular injury by adriamycin and puromycin (PAN). To investigate the potential roles of COX-2 metabolites, we studied mice with selective deletion of prostanoid receptors and generated conditionally immortalized podocyte lines from mice with either COX-2 deletion or overexpression. Podocytes that overexpressed COX-2 were virtually indistinguishable from wild-type podocytes but were significantly more sensitive to PAN-induced injury, produced more prostaglandin E(2) and thromboxane B(2), and had greater expression of prostaglandin E2 receptor subtype 4 (EP(4)) and thromboxane receptor (TP). Treatment of COX-2-overexpressing podocytes with a TP antagonist reduced apoptosis, but treatment with an EP(4) antagonist did not. In contrast, podocytes from COX-2-knockout mice exhibited increased apoptosis, markedly decreased cell adhesion, and prominent stress fibers. In vivo, selective deletion of podocyte EP(4) did not alter the increased sensitivity to adriamycin-induced injury observed in mice overexpressing podocyte COX-2. In contrast, genetic deletion of TP in these mice prevented adriamycin-induced injury, with attenuated albuminuria and foot process effacement. These results suggest that basal COX-2 may be important for podocyte survival, but overexpression of podocyte COX-2 increases susceptibility to podocyte injury, which is mediated, in part, by activation of the thromboxane receptor.

语种英语
WOS记录号WOS:000270248700018
项目编号DK51265 ; DK62794 ; DK79341
资助机构Department of Veterans Affairs ; National Institutes of Health
引用统计
被引频次:30[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
版本出版稿
条目标识符http://ir.bjmu.edu.cn/handle/400002259/62075
专题北京大学基础医学院_生理学与病理生理学系
北京大学基础医学院
作者单位1.Nashville Vet Affairs Hosp, Nashville, TN USA
2.Vanderbilt Univ, Sch Med, Div Nephrol, Nashville, TN 37232 USA
3.Vanderbilt Univ, Sch Med, Div Pathol, Nashville, TN 37232 USA
4.Vanderbilt Univ, Sch Med, George M OBrien Kidney & Urol Dis Ctr, Nashville, TN 37232 USA
5.Beijing Univ, Sch Med, Dept Physiol, Beijing 100871, Peoples R China
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GB/T 7714
Cheng, Huifang,Fan, Xiaofeng,Guan, Youfei,et al. Distinct Roles for Basal and Induced COX-2 in Podocyte Injury[J]. JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY,2009,20(9):1953-1962.
APA Cheng, Huifang,Fan, Xiaofeng,Guan, Youfei,Moeckel, Gilbert W.,Zent, Roy,&Harris, Raymond C..(2009).Distinct Roles for Basal and Induced COX-2 in Podocyte Injury.JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY,20(9),1953-1962.
MLA Cheng, Huifang,et al."Distinct Roles for Basal and Induced COX-2 in Podocyte Injury".JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY 20.9(2009):1953-1962.
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