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Upregulation of Urea Transporter UT-A2 and Water Channels AQP2 and AQP3 in Mice Lacking Urea Transporter UT-B

Janet D. Klein^*, Jeff M. Sands^*,, Liman Qian, Xiaodan Wang^* and Baoxue Yang

*Renal Division, Department of Medicine, and Department of Physiology, Emory University School of Medicine, Atlanta, Georgia; and Department of Medicine, University of California, San Francisco, San Francisco, California

Correspondence to Dr. Baoxue Yang, 1246 Health Sciences East Tower, University of California, San Francisco, San Francisco, CA 94143-0521. Phone: 415-476-8530; Fax: 415-665-3847; E-mail: byang{at}itsa.ucsf.edu

ABSTRACT. The UT-B urea transporter is the major urea transporter in red blood cells and kidney descending vasa recta. Humans and mice that lack UT-B have a mild urine-concentrating defect. Whether deletion of UT-B altered the expression of other transporter proteins involved in urinary concentration was tested. Fluorescence-based real-time reverse transcription–PCR and Northern blot analysis showed upregulation of the UT-A2 urea transporter and the aquaporin 2 (AQP2) and AQP3 water channel transcripts but no change in other urea transporters or AQP. Western blot analysis showed that UT-A2 protein abundance in the outer medulla of UT-B null mice increased to 122 ± 6% of wild-type control. AQP2 protein abundance increased to 177 ± 32% and 127 ± 7% in the outer and inner medulla, respectively, of UT-B null versus wild-type mice. The abundance of UT-A1, AQP1, renal outer medullary potassium channel, and NKCC2/BSC1 proteins were not significantly different between UT-B null and wild-type mice. The increases in AQP2 and AQP3 would reduce water loss and improve concentrating ability. The lack of UT-B does not result in a change in expression of urea transporters involved in urea reabsorption from the inner medullary collecting duct (UT-A1 and UT-A3). However, UT-B null mice have a selective increase in UT-A2 protein abundance. This may be an adaptive response to the loss of UT-B, because UT-B and UT-A2 are involved in different intrarenal urea recycling pathways.

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