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Research Article Free access | 10.1172/JCI1497

Induction of p21WAF1/CIP1/SDI1 in kidney tubule cells affects the course of cisplatin-induced acute renal failure.

J Megyesi, R L Safirstein, and P M Price

Department of Medicine, University of Texas Medical Branch, Galveston, Texas 77555, USA.

Find articles by Megyesi, J. in: PubMed | Google Scholar

Department of Medicine, University of Texas Medical Branch, Galveston, Texas 77555, USA.

Find articles by Safirstein, R. in: PubMed | Google Scholar

Department of Medicine, University of Texas Medical Branch, Galveston, Texas 77555, USA.

Find articles by Price, P. in: PubMed | Google Scholar

Published February 15, 1998 - More info

Published in Volume 101, Issue 4 on February 15, 1998
J Clin Invest. 1998;101(4):777–782. https://doi.org/10.1172/JCI1497.
© 1998 The American Society for Clinical Investigation
Published February 15, 1998 - Version history
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Abstract

The p21 protein is found in the nucleus of most cells at low levels and is induced to elevated levels after DNA damage, causing cell-cycle arrest. We have reported that p21 mRNA is rapidly induced to high levels in murine kidney after acute renal failure. The function(s) in the kidney of p21 induction in cisplatin-induced acute renal failure was studied with mice that are homozygous for a p21 gene deletion. After drug administration, as compared with their wild-type littermates, p21(-/-) mice display a more rapid onset of the physiologic signs of acute renal failure, develop more severe morphologic damage, and have a higher mortality. Therefore, the induction of p21 after cisplatin administration is a protective event for kidney cells. Using both bromodeoxyuridine incorporation and nuclear proliferating cell nuclear antigen detection, we found that cisplatin administration caused kidney cells to start entering the cell-cycle. However, cell-cycle progression is inhibited in wild-type mice, whereas kidney cells in the p21(-/-) mice progress into S-phase. We propose that p21 protects kidneys damaged by cisplatin by preventing DNA-damaged cells from entering the cell-cycle, which would otherwise result in death from either apoptosis or necrosis.

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  • Version 1 (February 15, 1998): No description

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