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Articles in PresS, published online ahead of print March 12, 2002
Am J Physiol Renal Physiol, 10.1152/ajprenal.00031.2002
Submitted on January 23, 2002
Accepted on February 28, 2002
1 Division of Nephrology and Hypertension, Department of Medicine; and Department of Cell and Developmental Biology, Oregon Health and Science University, Portland, OR, USA; Portland V.A. Medical Center, Portland, OR, USA
* To whom correspondence should be addressed. E-mail: cohend{at}ohsu.edu.
Although urea is considered to be a cell stressor even in renal medullary cells perpetually exposed to this solute in vivo by virtue of the renal concentrating mechanism, aspects of urea signaling resemble that of a peptide mitogen. Urea was compared to epidermal growth factor and hypertonic NaCl or hypertonic mannitol using a large-scale expression array-based approach. The expression profile in response to urea stress more closely resembled that of EGF treatment than hypertonic stress as determined by hierarchical cluster analysis; the effect of urea + NaCl was equidistant from that of either solute applied individually. Among the most highly urea- and hypertonicity-responsive transcripts were genes that had previously been shown to be responsive to these solutes, validating this approach. Increased expression of the transcription factor ATF-3 by urea was newly detected via expression array and confirmed via immunoblot analysis. We earlier noted abrogation of tonicity-dependent gene regulation by urea, primarily in a transient transfection-based model. We applied K-means cluster analysis to demonstrate that the genes most profoundly up- or down-regulated by hypertonic stress were partially restored toward basal levels in the presence of urea pretreatment. These global expression data are consistent with our earlier biochemical studies suggesting that urea affords cytoprotection in this context. In aggregate, these data strongly support the hypothesis that the urea effect in renal medullary cells resembles that of a peptide mitogen in terms of the adaptive program of gene expression and in terms of cytoprotection from hypertonicity.
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