Expression of Osteopontin in Chronic Potassium Depletion-induced Renal Injury.
- Author:
Ki Hwan HAN
1
;
Wan Young KIM
;
Hyun Kuk SONG
;
Jin KIM
Author Information
1. Department of Anatomy and MRC for Cell Death Disease Research Center, College of Medicine, The Catholic University of Korea, Seoul, Korea.
- Publication Type:Original Article
- Keywords:
Hypokalemia;
Renal injury;
Chemoattractant;
Osteopontin
- MeSH:
Animals;
Antibodies, Monoclonal;
Cell Membrane;
Cytoplasmic Vesicles;
Diet;
Epithelial Cells;
Epithelium;
Extremities;
Fibrosis;
Golgi Apparatus;
Hypertrophy;
Hypokalemia;
Immunohistochemistry;
Kidney;
Microscopy, Electron;
Osteopontin*;
Perfusion;
Potassium*;
Rats;
Rats, Sprague-Dawley
- From:Korean Journal of Anatomy
2004;37(1):67-74
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Osteopontin (OPN), a potent chemoattractant for the monocyte/macrophage infiltration, is highly upregulated in the renal tubular epithelium during various pathologic conditions associated with tubulointerstitial injury. The purpose of this study was to establish the distribution and localization of OPN in the tubulointerstitial injury induced by chronic potassium (K+) deprivation in the rat kidney. Sprague-Dawley rats were fed either a normal or a K+ -deficient diet for 2 weeks. Kidney tissues were preserved by in vivo perfusion with paraformaldehyde-lysine-periodate (PLP) and processed for light and electron microscope immunocytochemistry using monoclonal antibodies to OPN. K+ -depleted kidneys showed tubulointerstitial injury with renal hypertrophy, monocyte/macrophage infiltration, interstitial fibrosis, and OPN overexpression. OPN immunoreactivity was observed only in the descending thin limb (DTL) and the papillary surface epithelium (PSE) in the control kidney. However, the OPN labeling was observed not only in DTL and PSE but also in the thick ascending limb (TAL) in the K+ -depleted kidney. Electron microscopy revealed that OPN induced in the TAL cells was not located in the basal plasma membrane, but in the Golgi apparatus and in subapical cytoplasmic vesicles. There was no OPN expression in the epithelium of the collecting ducts, which showed marked morphological damages with mononuclear cell infiltration. These results demonstrate that chronic K+ -deprivation causes renal injury with the increased OPN expression in tubular epithelial cells. However, the localization of the induced OPN suggests other roles rather than a chemoattractant function in this renal injury model.
