遺伝性ネフローゼマウス(ICGN)の腎臓におけるマトリックスメタロプロテアーゼおよびマトリックスメタロプロテアーゼインヒビターの発現減少

  • UCHIO-YAMADA Kozue
    Department of Veterinary Sciences, National Institute of Infectious Diseases
  • MANABE Noboru
    Research Unit for Animal Life Sciences, Animal Resource Science Center, Department of Veterinary Medical Sciences, The University of Tokyo
  • GOTO Yasufumi
    Research Unit for Animal Life Sciences, Animal Resource Science Center, Department of Veterinary Medical Sciences, The University of Tokyo Unit of Anatomy and Cell Biology, Department of Animal Sciences, Kyoto University
  • ANANN Sayuri
    Research Unit for Animal Life Sciences, Animal Resource Science Center, Department of Veterinary Medical Sciences, The University of Tokyo Unit of Anatomy and Cell Biology, Department of Animal Sciences, Kyoto University
  • YAMAMOTO Yoshie
    Department of Veterinary Sciences, National Institute of Infectious Diseases
  • TAKANO Kaoru
    Department of Veterinary Sciences, National Institute of Infectious Diseases
  • OGURA Atsuo
    RIKEN Bioresource Center
  • MATSUDA Junichiro
    Department of Veterinary Sciences, National Institute of Infectious Diseases

書誌事項

タイトル別名
  • Decreased Expression of Matrix Metalloproteinases and Tissue Inhibitors of Metalloproteinase in the Kidneys of Hereditary Nephrotic (ICGN) Mice

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抄録

Matrix metalloporoteinases (MMPs), which are dominantly regulated by tissue inhibitors of metalloproteinase (TIMPs), play important roles in extracellular matrix (ECM) degradation and are involved in the progression of kidney diseases. In glomeruli and tubulointerstitum of hereditary nephrotic (ICR-derived glomerulonephritis: ICGN) mouse kidneys, hyper-accumulation of ECM components occurred, and MMP activity decreased. In the present study, because lower levels of MMP activity may contribute to the progression of renal fibrosis in ICGN mice, Western blotting analysis and immunohistochemical staining for MMPs and TIMPs were performed to verify the expression levels of these proteins. Levels of MMP-2, MMP-9, MT1-MMP, TIMP-1 and TIMP-2 in the kidneys were decreased in ICGN mice in comparison with normal ICR mice. These results indicate that small amounts and low levels of activity of MMPs cause the progression of renal fibrosis in ICGN mice.<br>

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