A Decrease in Glomerular Endothelial Cells and Endothelial-mesenchymal Transition during Glomerulosclerosis in the <i>Tensin2</i>-deficient Mice (ICGN strain)

この論文にアクセスする

著者

    • Kato Takashi
    • Department of Pathology, Faculty of Medicine, Kinki University|Division of Molecular Regenerative Medicine, Department of Biochemistry, Osaka University Graduate School of Medicine
    • Mizuno Shinya
    • Division of Virology, Department of Microbiology and Immunology, Osaka University Graduate School of Medicine|Division of Molecular Regenerative Medicine, Department of Biochemistry, Osaka University Graduate School of Medicine
    • Ito Akihiko
    • Department of Pathology, Faculty of Medicine, Kinki University

抄録

The ICR-derived glomerulonephritis (ICGN) mouse is a unique model of nephrotic syndrome, and albuminuria becomes evident in a neonatal stage, due to a genetic mutation of tensin2. We previously provided evidence that an apparent decrease in nephrin, caused by tensin2-deficiencient states, leads to podocytopathy, albuminuria and eventually, chronic renal failure. In general, glomerular endothelial cells (ECs) function as a barrier through tight attachment of glomerular basement membrane to podocytes, while decreased ECs can worsen renal failure. Nevertheless, it is still unknown whether glomerular ECs are altered under the tensin-2-deficient states during the manifestation of chronic renal failure. Herein, we examined the changes of glomerular ECs, with focus on the expression of PECAM-1 and VE-cadherin (EC-specific markers), or of <font face="roman">α</font>-SMA (myofibroblast marker) in this mouse model by histological methods. Compared with the non-nephrotic (+/nep) mice, the nephrotic (nep/nep) mice exhibited the reduced expression of PECAM-1, or of VE-cadherin, in glomerular area. Notably, some glomerular ECs showed the positive stainings for both PECAM-1 and <font face="roman">α</font>-SMA, suggesting endothelial-to-mesenchymal transition (EndoMT) during progression of glomerular sclerosis. This is the first report showing that a decrease in glomerular ECs, at least in part, via EndoMT is involved in tensin2-deficient pathological conditions.

収録刊行物

  • Acta Histochemica et Cytochemica

    Acta Histochemica et Cytochemica 47(6), 265-271, 2014

    日本組織細胞化学会

各種コード

  • NII論文ID(NAID)
    130004703745
  • 本文言語コード
    ENG
  • ISSN
    0044-5991
  • データ提供元
    J-STAGE 
ページトップへ