Tensin2 is important for podocyte-glomerular basement membrane interaction and integrity of the glomerular filtration barrier

DOI Web Site 被引用文献3件
  • Kozue Uchio-Yamada
    Laboratory of Animal Models for Human Diseases, National Institutes of Biomedical Innovation, Health and Nutrition, Ibaraki, Osaka, Japan
  • Keiko Yasuda
    Department of Nephrology, Osaka University Graduate School of Medicine, Suita, Osaka, Japan
  • Yoko Monobe
    Section of Laboratory Equipment, National Institutes of Biomedical Innovation, Health and Nutrition, Ibaraki, Osaka, Japan
  • Ken-ichi Akagi
    Section of Laboratory Equipment, National Institutes of Biomedical Innovation, Health and Nutrition, Ibaraki, Osaka, Japan
  • Osamu Suzuki
    Laboratory of Animal Models for Human Diseases, National Institutes of Biomedical Innovation, Health and Nutrition, Ibaraki, Osaka, Japan
  • Noboru Manabe
    Department of Human Sciences, Osaka International University, Moriguchi, Osaka, Japan

説明

<jats:p>Tensin2 (Tns2), an integrin-linked protein, is enriched in podocytes within the glomerulus. Previous studies have revealed that Tns2-deficient mice exhibit defects of the glomerular basement membrane (GBM) soon after birth in a strain-dependent manner. However, the mechanisms for the onset of defects caused by Tns2 deficiency remains unidentified. Here, we aimed to determine the role of Tns2 using newborn Tns2-deficient mice and murine primary podocytes. Ultrastructural analysis revealed that developing glomeruli during postnatal nephrogenesis exhibited abnormal GBM processing due to ectopic laminin-α<jats:sub>2</jats:sub>accumulation followed by GBM thickening. In addition, analysis of primary podocytes revealed that Tns2 deficiency led to impaired podocyte-GBM interaction and massive expression of laminin-α<jats:sub>2</jats:sub>in podocytes. Our study suggests that weakened podocyte-GBM interaction due to Tns2 deficiency causes increased mechanical stress on podocytes by continuous daily filtration after birth, resulting in stressed podocytes ectopically producing laminin-α<jats:sub>2</jats:sub>, which interrupts GBM processing. We conclude that Tns2 plays important roles in the podocyte-GBM interaction and maintenance of the glomerular filtration barrier.</jats:p>

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