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Cellular receptors for matrix proteins in normal human kidney and human mesangial cells

F G Cosio1, D D Sedmak, N S Nahman

  • 1Department of Internal Medicine and Pathology, Ohio State University, Columbus.

Kidney International
|November 1, 1990
PubMed

Insights

Very late antigens (VLA) distribution was studied in human kidneys and mesangial cells. VLA-3 is predominant in glomeruli, while VLA-5 mediates mesangial cell binding to fibronectin.

Area of Science:

  • Nephrology
  • Cell Biology
  • Immunology

Background:

  • Cell adhesion molecules, specifically very late antigens (VLA), play crucial roles in cellular interactions within tissues.
  • Understanding VLA distribution and function in the kidney is essential for comprehending glomerular and mesangial cell behavior.

Purpose of the Study:

  • To investigate the distribution of VLA proteins in normal human kidney glomeruli and cultured mesangial cells (MC).
  • To assess the functional significance of VLA proteins, particularly their role in MC adhesion to fibronectin (FN).

Main Methods:

  • Immunoperoxidase staining of normal human kidney and MC using monoclonal antibodies against VLA proteins.
  • Functional assays evaluating MC binding to FN-coated surfaces and phagocytosis of FN-coated beads.
  • Affinity chromatography and immunoprecipitation to characterize MC FN-binding proteins and VLA proteins.

Main Results:

  • VLA-3 was identified as the predominant VLA protein in the human glomerulus and on MC, localizing to the mesangium and glomerular cell surfaces.
  • VLA-5, an FN-specific receptor, was found on MC and glomerular endothelial cells.
  • MC binding to FN was mediated by VLA-5 and inhibited by anti-VLA-5 antibodies, anti-FN antibodies, and RGD peptides.
  • MC demonstrated binding and phagocytosis of FN-coated beads, inhibited by purified FN.

Conclusions:

  • The distribution of VLA-3 suggests its primary role in glomerular cell adhesion to basement membranes and extracellular matrix.
  • VLA-5 functions as a key receptor mediating MC adhesion to fibronectin and potentially phagocytosis of FN-associated complexes.

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