Localization of proliferative and apoptotic cells in the kidneys of ICR-derived glomerulonephritis (ICGN) mice

Citation
M. Yamaguchi et al., Localization of proliferative and apoptotic cells in the kidneys of ICR-derived glomerulonephritis (ICGN) mice, J VET MED S, 63(7), 2001, pp. 781-787
Citations number
32
Categorie Soggetti
Veterinary Medicine/Animal Health
Journal title
JOURNAL OF VETERINARY MEDICAL SCIENCE
ISSN journal
09167250 → ACNP
Volume
63
Issue
7
Year of publication
2001
Pages
781 - 787
Database
ISI
SICI code
0916-7250(200107)63:7<781:LOPAAC>2.0.ZU;2-Y
Abstract
The ICR-derived glomerulonephritis (ICGN) mouse is a novel inbred mouse str ain with a hereditary nephrotic syndrome, considered to be a good model of human idiopathic nephrotic syndrome and develops proteinuria, hypoproteinem ia and anemia. In the present study, we compared the cell kinetics in the k idneys of ICGN mice with age-matched ICR mice as normal controls. The proli ferating cells were visualized by 5-bromo-2 ' -deoxyuridine, labeling, and apoptotic cells were determined by terminal deoxynucleotidyl transferase-me diated biotinylated deoxyuridine triphosphate nick end-labeling. Many proli ferating epithelial cells of renal tubules, glomerular mesangial cells and tublointerstitial fibroblast-like cells were observed in the kidneys of ICG N mice, but no proliferating cells were seen in the kidneys of ICR mice. Ap optotic cells had round nuclei, and were observed only in the tubulointerst itium in the kidneys of ICGN mice but not in that of controls. The prolifer ation of renal tubular epithelial cells may represent a compensatory respon se, and that of mesangial and fibroblast-like cells may play a pathogenic r ole in nephrotic syndrome. Apoptosis in tubulointerstitial cells with round nuclei may have been erythropoietin-producing cells, and probably caused a nemia.