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学科主题: 基础医学
题名:
Distinct Roles for Basal and Induced COX-2 in Podocyte Injury
作者: 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
发表日期: 2009-09-01
DOI: 10.1681/ASN.2009010039
卷: 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
所属项目编号: DK51265 ; DK62794 ; DK79341
项目资助者: Department of Veterans Affairs ; National Institutes of Health
WOS记录号: WOS:000270248700018
Citation statistics:
内容类型: 期刊论文
版本: 出版稿
URI标识: http://ir.bjmu.edu.cn/handle/400002259/62075
Appears in Collections:基础医学院_生理学与病理生理学系_期刊论文

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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

Recommended Citation:
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.
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