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Division of Nephrology, Hypertension, and Clinical Pharmacology and Division of Molecular Medicine, Department of Medicine, Oregon Health Sciences University and the Portland Veterans Affairs Medical Center, Portland, Oregon 97201
Urea treatment (100-300 mM) increased
expression of the oxidative stress-responsive transcription factor,
Gadd153/CHOP, at the mRNA and protein levels (at 
4 h) in renal
medullary mIMCD3 cells in culture, whereas other solutes did not.
Expression of the related protein, CCAAT/enhancer-binding protein
(C/EBP-
), was not affected, nor was expression of the sensor of
endoplasmic reticulum stress, grp78. Urea modestly increased Gadd153
transcription by reporter gene analysis but failed to influence Gadd153
mRNA stability. Importantly, upregulation of Gadd153 mRNA and protein expression by urea was antioxidant sensitive. Accordingly, urea treatment was associated with oxidative stress, as quantitated by
intracellular reduced glutathione content in mIMCD3 cells. In addition,
antioxidant treatment partially inhibited the ability of urea to
activate transcription of an Egr-1 luciferase reporter gene. Therefore
oxidative stress represents a novel solute-signaling pathway in the
kidney medulla and, potentially, in other tissues.
hypertonic; kidney; cell culture; mouse; Egr-1; sodium chloride
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