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1 Pediatrics, University of Cincinnati Children Medical Center, Cincinnati, OH, USA
2 Medicine, University of Cincinnati, Cincinnati, OH, USA
3 Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA
4 Medicine, University of Cincinnati, Cincinnati, OH, USA; Medical Research, Veterans Hospital, Cincinnati, OH, USA
* To whom correspondence should be addressed. E-mail: manoocher.soleimani{at}uc.edu.
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 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 4 fold at 24 hours of reperfusion. The stathmin mRNA did not increase in sodium-depleted animals or animal with active persistent injury secondary to cis-platinum. Immunofluorescent labeling demonstrated that the expression of stathmin increased dramatically at 48 hours of reperfusion. Labeling with antibodies to stathmin and proliferating cell nuclear antigen (PCNA) indicate that the expression of stathmin is induced prior to the upregulation of PCNA, and that all PCNA positive cells express stathmin. Double immunofluorescent labeling demonstrated the co-localization of stathmin with vimentin, a marker of dedifferentiated cells. Stathmin expression was also significantly enhanced in acute tubular necrosis in humans. Based on 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.
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