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Distinct roles for basal and induced COX-2 in podocyte injury.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Cheng, Huifang Fan, Xiaofeng Guan, Youfei Moeckel, Gilbert W. Zent, Roy Harris, Raymond C.
Description	Country affiliation: United States Author Affiliation: Cheng H ( Division of Nephrology, Vanderbilt University School of Medicine and Nashville Veterans Affairs Hospital, Nashville, TN 37232, USA.)
Abstract	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 E(2) 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.
File Format	HTM / HTML
ISSN	10466673
e-ISSN	15333450
DOI	10.1681/ASN.2009010039
Journal	Journal of the American Society of Nephrology
Issue Number	9
Volume Number	20
Language	English
Publisher	American Society of Nephrology
Publisher Date	2009-09-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Discipline Nephrology Cyclooxygenase 2 Metabolism Glomerulonephritis Pathology Physiopathology Podocytes Physiology Albuminuria Chemically Induced Animals Antibiotics, Antineoplastic Toxicity Apoptosis Drug Effects Cell Adhesion Cell Line, Transformed Cell Survival Genetics Dinoprostone Pharmacology Doxorubicin Mice Mice, Inbred Strains Mice, Transgenic Puromycin Rna, Messenger Receptors, Prostaglandin E Receptors, Thromboxane Thromboxanes Research Support, N.i.h., Extramural Research Support, U.s. Gov't, Non-p.h.s.
Content Type	Text
Resource Type	Article
Subject	Nephrology

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Distinct Roles for Basal and Induced COX-2 in Podocyte Injury

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