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This Article Full Text Full Text (PDF) All Versions of this Article: 293/6/F1898    most recent 00360.2007v1 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 Google Scholar Google Scholar Articles by Liu, H. Articles by Yang, T. Search for Related Content PubMed PubMed Citation Articles by Liu, H. Articles by Yang, T.

Developmental regulation of calcineurin isoforms in the rodent kidney: association with COX-2

¹Division of Nephrology, University of Utah and Veterans Affairs Medical Center, Salt Lake City, Utah; ²Department of Nephrology, Shandong University Medical School, Jinan, Shandong Province, Peoples Republic of China; ³Cellular Biology and Anatomy, Medical College of Georgia, Augusta; and ⁴Medical Research Service, Veterans Affairs Medical Center, Augusta, Georgia

Submitted 1 August 2007 ; accepted in final form 5 September 2007

Calcineurin (Cn)-A-deficient mice develop abnormalities of postnatal kidney development, similar to that of cyclooxygenase (COX)-2-deficient mice. The present study was undertaken to examine expression and regulation of Cn isoforms in the developing kidney during the postnatal period and further characterize the relationship between Cn and COX-2. The protein expressions of all three Cn isoforms, including Cn-A, -Aβ, and -B, as determined by immunoblotting, increased in parallel in the first postnatal week and declined gradually with age. Renal Cn-A and -Aβ mRNA expressions were both developmentally regulated in the same fashion as their protein expressions, whereas renal Cn-B1 mRNA was not obviously induced in the first postnatal week. Immunohistochemistry demonstrated colocalization of Cn-A, Cn-Aβ, and COX-2 in the same cells of thick ascending limb and macula densa. Administration with cyclosporine A (2.5 mg·kg^–1·day^–1) during the postnatal period remarkably suppressed renal COX-2 expression as assessed by both immunoblotting and immunohistochemistry. Deletion of Cn-A but not Cn-Aβ in mice significantly reduced renal COX-2 expression at the postnatal period. Together, these data suggest that renal Cn isoforms are subject to normal developmental regulation and they may play a role in postnatal kidney development via interaction with COX-2.

cyclooxygenase-2; postnatal kidney development; cyclosporine A