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Am J Physiol Renal Physiol (September 16, 2003). doi:10.1152/ajprenal.00099.2003
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Submitted on March 7, 2003
Accepted on September 11, 2003

Low endogenous glucocorticoid allows induction of kidney cortical cyclooxygenase-2 during postnatal rat development

Kirsten Madsen1, Jane Stubbe1, Tianxin Yang2, Ole Skott1, Sebastian Bachmann3, and Boye L. Jensen1*

1 Department of Physiology and Pharmacology, University of Southern Denmark, Odense, Denmark
2 Division of Nephrology, University of Utah School of Medicine and Salt Lake Veterans Affairs Medical Center, Salt Lake City, Utah, USA
3 Department of Anatomy, Humboldt University, Charite, Berlin, Germany

* To whom correspondence should be addressed. E-mail: bljensen{at}health.sdu.dk.

In the second to fourth postnatal weak cyclooxygenase-2 (COX-2) is induced in the rat kidney cortex where it is critically involved in final stages of kidney development. We examined whether changes in circulating gluco- or mineralocorticosteroids or in their renal receptors regulate postnatal COX-2 induction. Plasma corticosterone concentration peaked at birth, decreased to low levels at days 3-13 and increased to adult levels from day 22. Aldosterone peaked at birth and then stabilized at adult levels. Gluco- and mineralocorticoid receptor (GR and MR) mRNAs were expressed stably in kidney before, during and after COX-2 induction. 11 {beta}-hydroxysteroid dehydrogenase 2 (11 {beta}HSD-2) was induced shortly after birth and was widely distributed in the whole collecting duct system in the suckling period and then returned to an adult pattern. Supplementation with corticosterone (20 mg/kg*day) or GR-specific dexamethasone (1 mg/kg*day) during low endogenous corticosterone suppressed renal COX-2 mRNA and protein and led to a restricted distribution of COX-2 immunolabeling. The ability of glucocorticoids to affect COX-2 was reflected in co-localization of GR-{alpha} and COX-2 immunoreactivity and mRNAs in thick ascending limb of Henles loop. The MR-antagonist, potassium canrenoate (20 mg/kg*day) enhanced COX-2 expression from days 5-10, but low, MR-specific, concentrations of DOCA (1 mg/kg*day) had no effect on COX-2. Renomedullary interstitial cells expressed GR-{alpha} and COX-2. Dexamethasone suppressed COX-2 in these cells. Thus,low plasma concentrations of corticosterone allowed for cortical and medullary COX-2 induction during postnatal kidney development. Increased circulating glucocorticoid in the postnatal period may damage late renal development through inhibition of COX-2.




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