Articles in PresS. Am J Physiol Renal Physiol (October 28, 2003). 10.1152/ajprenal.00173.2003
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RENAL RETINOID SYSTEM: TIME-DEPENDENT ACTIVATION IN EXPERIMENTAL GLOMERULONEPHRITIS
Sabine Liebler, Birgit Überschär, Helen Kübert, Stefanie Brems, Anna Schnitger1, Miki Tsukada1, Christos C. Zouboulis1, Eberhard Ritz and Jürgen Wagner
Department of Nephrology, University of Heidelberg, 69115 Heidelberg, Germany 1
Department of Dermatology, University Medical Center Benjamin Franklin,
The Free University of Berlin, 14195 Berlin, Germany
Running head: Renal Retinoid System in Acute Glomerulonephritis
Address for Correspondence: Sabine Liebler Department of Nephrology University Hospital University of Heidelberg Bergheimer Strasse 56 a D-69115 Heidelberg Tel: +49 6221 911211 Fax: +49 6221 911279 E-mail:
[email protected]
Copyright (c) 2003 by the American Physiological Society.
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Abstract Retinoids reduce renal damage in rat experimental glomerulonephritis. It is unknown, however, how local and systemic retinoid pathways respond to renal injury. We, therefore, examined the extrarenal and glomerular expression of the retinol (RoDH) and retinal (RalDH) dehydrogenases 1 and 2 as well as the expression of the retinoic acid (RAR) and retinoid X (RXR) receptor subtypes α, β, and γ at several times in acute anti-Thy1.1nephritis (THY-GN). Furthermore, we investigated serum and glomerular retinoid concentration patterns. On day 3, 7, and 14 we compared non-nephritic rats (control group; CON) to THY-GN rats. Systolic blood pressure and glomerular cell count were significantly higher in THY-GN rats on day 7 and 14 (p
