| First Author | Kuehn EW | Year | 2002 |
| Journal | Am J Physiol Renal Physiol | Volume | 283 |
| Issue | 6 | Pages | F1326-36 |
| PubMed ID | 12388382 | Mgi Jnum | J:80687 |
| Mgi Id | MGI:2446940 | Doi | 10.1152/ajprenal.00166.2002 |
| Citation | Kuehn EW, et al. (2002) Kidney injury molecule-1 expression in murine polycystic kidney disease. Am J Physiol Renal Physiol 283(6):F1326-36 |
| abstractText | Kidney injury molecule-1 (Kim-1) is a type 1 membrane protein maximally upregulated in proliferating and dedifferentiated tubular cells after renal ischemia. Because epithelial dedifferentiation, proliferation, and local ischemia may play a role in the pathophysiology of autosomal dominant polycystic kidney disease, we investigated Kim-1 expression in a mouse model of this disease. In the Pkd2(WS25/-) mouse model for autosomal dominant polycystic kidney disease, cystic kidneys show markedly upregulated Kim-1 levels compared with 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 alpha-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 dedifferentiation of epithelial cells and may play a role in the development of interstitial fibrosis. |
