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Articles in PresS, published online ahead of print August 15, 2001
Am J Physiol Renal Physiol, 10.1152/ajprenal.0358.2000
Submitted on January 1, 2001
Accepted on July 3, 2001
1 Divisions of Nephrology and Molecular Medicine, Oregon Health Sciences University, Portland, OR, USA
2 Department of Medicine, University of Massachusetts Medical School, Worcester, MA, USA
3 Department of Molecular Biology and Applied Physiology, Tohoku University School of Medicine, Sendai, Miyagi, Japan
4 Divisions of Nephrology and Molecular Medicine, Oregon Health Sciences University, Portland, OR, USA; Division of Nephrology, Portland Veterans Affairs Medical Center, Portland, OR, USA
* To whom correspondence should be addressed. E-mail: cohend{at}ohsu.edu.
Epithelial cells derived from the mammalian kidney medulla are responsive to urea at the levels of signal transduction and gene regulation. Hybridization of RNA harvested from control- and urea-treated murine renal medullary mIMCD3 cells with a cDNA expression array encoding stress-responsive genes suggested that HO-1 mRNA was upregulated by urea. RNase protection assay confirmed this upregulation; hypertonicity also increased HO-1 mRNA expression but neither hypertonic NaCl nor urea were effective in the non-renal 3T3 cell line. The effect upon HO-1 expression appeared to be transcriptionally mediated based upon mRNA half-life studies and reporter gene analyses using the promoters of both human and chicken HO-1. Although urea signaling resembles that of heavy metal signaling in other contexts, the effect of urea upon HO-1 transcription was independent of the cadmium response element in this promoter. Urea-inducible HO-1 expression was sensitive to antioxidants but not to scavengers of nitric oxide. Urea also upregulated HO-1 protein expression and pharmacological inhibition of HO-1 action with zinc protoporphyrin sensitized mIMCD3 cells to the adverse effects of hypertonicity but not to urea. Coupled with the prior observation of others that HO-1 expression increases along the renal corticomedullary gradient, these data suggest that HO-1 expression may comprise an element of the adaptive response to hypertonicity and/or urea in renal epithelial cells.
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