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Am J Physiol Cell Physiol 286: C1203-C1211, 2004. First published December 30, 2003; doi:10.1152/ajpcell.00432.2003
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REPORTS

Identification of stathmin as a novel marker of cell proliferation in the recovery phase of acute ischemic renal failure

Kamyar Zahedi,1 Zhaohui Wang,3 Sharon Barone,3 Kathy Tehrani,1 Naoko Yokota,2 Snezana Petrovic,3,4 Hamid Rabb,2 and Manoocher Soleimani3,4

1Division of Nephrology and Hypertension, Department of Pediatrics, Children Hospital Medical Center, Cincinnati, Ohio 45229; 2Division of Nephrology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21218; 3Division of Nephrology and Hypertension, Department of Medicine, University of Cincinnati, Cincinnati 45267; and 4Veterans Affairs Medical Center, Cincinnati, Ohio 45220

Submitted 6 October 2003 ; accepted in final form 29 December 2003

ABSTRACT

Ischemic renal injury can be classified into the initiation and extension phase followed by the recovery phase. The recovery phase is characterized by increased dedifferentiated and mitotic cells in the damaged tubules. Suppression subtractive hybridization was performed by using RNA from normal and ischemic kidneys to identify the genes involved in the physiological response to ischemia-reperfusion injury (IRI). The expression of stathmin mRNA increased by fourfold at 24 h of reperfusion. The stathmin mRNA did not increase in sodium-depleted animals or in animals with active, persistent injury secondary to cis-platinum. Immunofluorescent labeling demonstrated that the expression of stathmin increased dramatically at 48 h of reperfusion. Labeling with antibodies to stathmin and proliferating cell nuclear antigen (PCNA) indicates that the expression of stathmin was induced before the upregulation of PCNA and that all PCNA-positive cells expressed stathmin. Double immunofluorescent labeling demonstrated the colocalization of stathmin with vimentin, a marker of dedifferentiated cells. Stathmin expression was also significantly enhanced in acute tubular necrosis in humans. On the basis of its induction profile in IRI, the data indicating its enhanced expression in proliferating cells and regenerating organs, we propose that stathmin is a marker of dedifferentiated, mitotically active epithelial cells that may contribute to tubular regeneration and could prove useful in distinguishing the injury phase from recovery phase in IRI.

acute renal failure; acute tubular necrosis; ischemia-reperfusion injury; cis-platinum nephrotoxicity; sodium depletion; tubule regeneration


Address for reprint requests and other correspondence: K. Zahedi, Division of Nephrology and Hypertension, Children's Hospital Research Foundation, 3333 Burnet Ave., Cincinnati, OH 45229-3039 (E-mail: Zahek0{at}cchmc.org) or M. Soleimani, Division of Nephrology and Hypertension, Dept. of Medicine, Univ. of Cincinnati, 231 Albert Sabin Way, MSB 259G, Cincinnati OH 45267-0585 (E-mail: Manoocher.soleimani{at}uc.edu).




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