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Articles in PresS, published online ahead of print May 29, 2002
Am J Physiol Renal Physiol, 10.1152/ajprenal.00078.2002
Submitted on February 25, 2002
Accepted on May 14, 2002
1 Department of Internal Medicine, University of Arkansas for Medical Sciences and Department of Veterans Affairs Medical Center, Little Rock, AR, USA; Internal Medicine, Department of Veterans Affairs Medical Center, Little Rock, AR, USA
* To whom correspondence should be addressed. E-mail: pricepeterm{at}uams.edu.
Recovery from injury is usually accompanied by cell replication in which new cells replace those irreparably damaged. After acute renal failure, normally quiescent kidney cells enter the cell cycle, which in tubule segments, is accompanied by the induction of cell cycle inhibitors. We found that after acute renal failure induced either by cisplatin injection or renal ischemia, induction of the p21 cyclin-dependent kinase (cdk) inhibitor is protective. Mice lacking this gene developed more widespread kidney cell death, more severe renal failure, and had reduced survival, compared with mice with a functional p21 gene. Here we show induction of 14-3-3
, a regulator of G2 to M transition, after acute renal failure. Our findings using both in vivo and in vitro models of acute renal failure show that this protein likely helps to coordinate cell cycle activity to maximize recovery of renal epithelial cells from injury and reduce the extent of the injury itself. Since in terminally differentiated cells, these proteins are highly expressed only after injury, we propose that cell cycle coordination by induction of these proteins could be a general model of tissue recovery to stress and injury.
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