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Articles in PresS, published online ahead of print July 24, 2002
Am J Physiol Renal Physiol, 10.1152/ajprenal.00166.2002
Submitted on April 30, 2002
Accepted on July 12, 2002
1 Renal Unit, Department of Medicine, Massachusetts General Hospital, Charlestown, MA, USA
2 Section of Nephrology, Yale University School of Medicine, New Haven, CT, USA
3 Renal Unit, Department of Medicine, Massachusetts General Hospital, Charlestown, MA, USA; Division of Health Sciences and Technology, Harvard-Massachusetts Institute of Technology, Cambrige, MA, USA
* To whom correspondence should be addressed. E-mail: joseph_bonventre{at}hms.harvard.edu.
Kidney Injury Molecule-1 (Kim-1) is a type 1 membrane protein maximally upregulated in proliferating and de-differentiated tubular cells after renal ischemia. Since epithelial de-differentiation, proliferation and local ischemia may play a role in the pathophysiology of autosomal dominant polycystic kidney disease (ADPKD), we investigated Kim-1 expression in a mouse model of this disease. In the Pkd2WS25/- mouse model for ADPKD, cystic kidneys show markedly upregulated Kim-1 levels compared to noncystic control kidneys. Kim-1 is present in a subset of cysts of different sizes and segmental origins and in clusters of proximal tubules near cysts. Kim-1 expressing tubular cells show decreased complexity and quantity of basolateral staining for Na,K-ATPase. Other changes in polarity characteristic of ischemic injury are not present in Kim-1 expressing pericystic tubules. Polycystin 2 expression is preserved in Kim-1 expressing tubules. The interstitium surrounding Kim-1 expressing tubules shows high proliferative activity and staining for smooth muscle 
-actin, characteristic of myofibroblasts. Although the functional role of the protein in cysts remains unknown, Kim-1 expression in tubules is strongly associated with partial de-differentiation of epithelial cells and may play a role in the development of interstitial fibrosis.
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