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1 Department of Physiology, Medical College of Wisconsin, Milwaukee, WI, USA
2 Department of Medicine, Medical College of Wisconsin, Milwaukee, WI, USA
3 Department of Physiology, Pontificia Universidad Catolica de Chile, Santiago, Chile
4 Department of Genome Sciences, University of Washington, Seattle, WA, USA
* To whom correspondence should be addressed. E-mail: dbasile{at}mcw.edu.
Recovery from ischemic acute renal failure involves a well described regenerative process; however recovery from ARF also results in a predisposition to a progressive renal disease that is not well understood. This study sought to identify alterations in renal gene expression in post-ischemic recovered animals that might play important roles in this progressive disorder. RNA isolated from sham-operated control rats, or rats 35 days following recovery from bilateral I/R injury were compared using a cDNA microarray containing ~2000 known rat genes. A reference hybridization strategy was utilized to define a 99.9% interval and to identify 16 genes that were persistently altered following recovery from I/R injury (12 up-regulated and 4 down-regulated). Real Time PCR verified the altered expression of 6 of 8 genes that had been positively identified. Several genes that were identified had not previously been evaluated within the context of acute renal failure. S100A4, a specific marker of fibroblasts, was identified in a population of interstitial cells that were present post-ischemic injury. S100A4-positive cells were also identified in tubular cells at earlier time points post-ischemia. Genes associated with calcification including osteopontin and matrix Gla protein were also enhanced post-ischemic injury. Several proinflammatory genes were identified, including Complement C4 were enhanced in post ischemic tissues. Conversely, renal kallikrein expression was specifically reduced in the post-ischemic kidney. In summary, genes with known inflammatory, remodeling and vasoactive activities were identified in rat kidneys following recovery from ARF, some of which may play a role in altering long-term renal function following recovery from ARF.
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