Localization of Proliferative and Apoptotic Cells in the Kidneys of ICR-Derived Glomerulonephritis(ICGN) Mice.

  • YAMAGUCHI Misuzu
    Unit of Anatomy and Cell Biology, Department of Animal Sciences, Kyoto University
  • MANABE Noboru
    Unit of Anatomy and Cell Biology, Department of Animal Sciences, Kyoto University
  • UCHIO-YAMADA Kozue
    Unit of Anatomy and Cell Biology, Department of Animal Sciences, Kyoto University
  • AKASHI Naotsugu
    Unit of Anatomy and Cell Biology, Department of Animal Sciences, Kyoto University
  • YAMAMOTO Yoshie
    Department of Veterinary Sciences, National Institute of Infectious Diseases
  • OGURA Atsuo
    Department of Veterinary Sciences, National Institute of Infectious Diseases
  • MIYAMOTO Hajime
    Unit of Anatomy and Cell Biology, Department of Animal Sciences, Kyoto University

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The ICR-derived glomerulonephritis (ICGN) mouse is a novel inbred mouse strain with a hereditary nephrotic syndrome, considered to be a good model of human idiopathic nephrotic syndrome and develops proteinuria, hypoproteinemia and anemia. In the present study, we compared the cell kinetics in the kidneys of ICGN mice with age-matched ICR mice as normal controls. The proliferating cells were visualized by 5-bromo-2'-deoxyuridine labeling, and apoptotic cells were determined by terminal deoxynucleotidyl transferase-mediated biotinylated deoxyuridine triphosphate nick end-labeling. Many proliferating epithelial cells of renal tubules, glomerular mesangial cells and tublointerstitial fibroblast-like cells were observed in the kidneys of ICGN mice, but no proliferating cells were seen in the kidneys of ICR mice. Apoptotic cells had round nuclei, and were observed only in the tubulointerstitium in the kidneys of ICGN mice but not in that of controls. The proliferation of renal tubular epithelial cells may represent a compensatory response, and that of mesangial and fibroblast-like cells may play a pathogenic role in nephrotic syndrome. Apoptosis in tubulointerstitial cells with round nuclei may have been erythropoietin-producing cells, and probably caused anemia.

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