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1 Divisions of Nephrology and Molecular Medicine, Oregon Health Sciences University and the 4 Portland Veterans Affairs Medical Center, Portland, Oregon 97201; 2 Department of Medicine, University of Massachusetts Medical School, Worcester, Massachusetts 01655; and 3 Department of Molecular Biology and Applied Physiology, Tohoku University School of Medicine, Sendai, Miyagi, Japan
First Published August 15, 2001;
10.1152/ajprenal. 00358.2001.
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 inner medullary collecting duct
(mIMCD3) cells with a cDNA expression array encoding stress-responsive genes suggested that heme oxygenase (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 nonrenal 3T3 cell line. The effect on HO-1
expression appeared to be transcriptionally mediated on the basis of
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 on 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.
sodium chloride; osmotic; oxidative stress; transcription
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