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This Article Full Text Full Text (PDF) All Versions of this Article: 292/1/F278    most recent 00089.2006v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (3) Citing Articles via Google Scholar Google Scholar Articles by Nasrallah, R. Articles by Hébert, R. L. Search for Related Content PubMed PubMed Citation Articles by Nasrallah, R. Articles by Hébert, R. L.

Renal prostaglandin E₂ receptor (EP) expression profile is altered in streptozotocin and B6-Ins2^Akita type I diabetic mice

Department of Cellular and Molecular Medicine, Kidney Research Centre, Faculty of Medicine, University of Ottawa, Ottawa, Ontario, Canada

Submitted 16 March 2006 ; accepted in final form 28 August 2006

The homeostatic function of prostaglandin E₂ (PGE₂) is dependent on a balance of EP receptor-mediated events. A disruption in this balance may contribute to the progression of renal injury. Although PGE₂ excretion is elevated in diabetes, the expression of specific EP receptor subtypes has not been studied in the diabetic kidney. Therefore, the purpose of this study was to characterize the expression profile of four EP receptor subtypes (EP_1-4) in 16-wk streptozotocin (STZ) and B6-Ins2^Akita type I diabetic mice. In diabetic mice, the ratio of kidney weight to body weight was increased twofold compared with controls, blood glucose was elevated, but urine albumin was only increased in B6-Ins2^Akita mice. The excretion of PGE₂ and its metabolite was augmented two- to fourfold as determined by enzyme immunoassay. Accordingly, renal cyclooxygenases were also increased in diabetic mice, with isoform-specific and regional differences in each model. Finally, there was altered EP_1-4 receptor expression in diabetic kidneys, with significant differences between STZ and B6-Ins2^Akita mice (fold-control). In STZ mice, cortical EP₁ increased by 1.6, EP₃ increased by 2.3, and EP₄ decreased by 0.63; yet in B6-Ins2^Akita mice, cortical EP₁ increased by 2.4, but there was a general decrease in the remaining subtypes. Similarly, in the STZ medulla EP₃ increased by 3.6, but both EP₁ and EP₃ increased by 5.5 and 1.95, respectively, in B6-Ins2^Akita mice. Therefore, knowing the pattern of change in relative EP receptor expression in the kidney could be useful in identifying specific EP targets for the prevention of various components of diabetic kidney disease.

cyclooxygenase; real-time reverse transcriptase polymerase-chain reaction; renal EP receptors; streptozotocin-diabetic mice

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