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1 Department of Physiology, University of Arizona, Tucson, AZ, USA
2 Biomedical Engineering Program, University of Arizona, Tucson, AZ, USA
* To whom correspondence should be addressed. E-mail: brooksh{at}email.arizona.edu.
Mice that lack the aquaporin-1 gene (AQP1) lack a functional countercurrent multiplier mechanism, fail to concentrate the inner medullary (IM) interstitium and present with a urinary concentrating defect. In this study we use DNA microarrays to identify the gene expression profile of the IM of AQP1 null mice and corresponding changes in gene expression resulting from a loss of a hypertonic medullary interstitium. An ANOVA analysis model, CARMA, was used to isolate the knockout effect while taking into account experimental variability associated with microarray studies. In this study 5701
genes out of the possible ~12000 genes on the array were included in the ANOVA. 531 genes were identified as demonstrating a 
1.5 fold up or down regulation between the wild type and knock-out groups. We randomly selected 35 genes for confirmation by real-time PCR and 29 of the 35 genes were confirmed using this method. The overall pattern of gene expression in the AQP1 null mice was one of down-regulation compared to gene expression in the renal medullae of the wild type mice. Heat shock proteins 105 and 94, aldose reductase, adenylate kinase 2, aldolase B, aldehyde reductase 6, and p8 were decreased in the AQP1 null mice. Carboxylesterase 3, matrilin 2, lipocalin 2 and transforming growth factor-
were increased in IM of AQP1 null mice. In addition, we observed a loss of vasopressin type 2 receptor mRNA expression in renal medullae of the AQP1 null mice. Thus, the loss of the hyperosmotic renal interstitium, due to a loss of the concentrating mechanism, drastically altered not only the phenotype of these animals but also their renal medullary gene expression profile.
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