Localization or extracellular matrix receptors in ICGN mice, a strain of mice with hereditary nephrotic syndrome

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  • UCHIO-YAMADA Kozue
    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
  • YAMAGUCHI Misuzu
    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
  • GOTO Yasufumi
    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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タイトル別名
  • Localization of Extracellular Matrix Receptors in ICGN Mice, a Strain of Mice with Hereditary Nephrotic Syndrome.

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Fibrotic degeneration was examined in the kidneys of ICR-derived glomerulonephritis (ICGN) mice, a novel inbred mouse line with a hereditary nephrotic syndrome of unknown etiology considered to be a good model of human idiopathic nephrotic syndrome. In the present study, we histochemically revealed changes in accumulation of extracellular matrix (ECM) components and in localization of integrins, cellular receptors for ECM, in the kidneys of ICGN mice with the progression of renal failure. Excessive accumulation of basement membrane (laminin and collagen IV) and interstitial (type III collagen) ECM components were demonstrated in the glomeruli and tubulointerstitum of ICGN mice. Marked deposition of type I collagen and tenascin was seen only in the glomeruli of ICGN mice but not in those of ICR mice as normal controls. Increased expression of integrin α1-, α2-, α5- and β1-subunits in glomeruli with fibrotic degeneration and abnormal distribution of α6-subunit were noted in the kidneys of ICGN mice. Excessive laminin, a ligand of α6β1-integrin, was demonstrated on the tubular basement membrane, but α6-subunit diffusely disappeared on the basal side of the tubular epithelial cells. We presumed that abnormal integrin expression in renal tubules causes epithelial cell detachment, and consequently tubular nephropathy, and results in disorder of ECM metabolism causing excessive accumulation of ECM components in the kidneys of ICGN mice.

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