VLA-5-mediated interaction with fibronectin induces cytokine production by human chondrocytes

Biochem Biophys Res Commun. 1996 Feb 6;219(1):261-5. doi: 10.1006/bbrc.1996.0215.

Abstract

Adhesion molecules of the integrin family, including very late activation antigens (VLA), have been implicated in various cellular functions. In this study, we investigated the contribution of integrin-mediated interaction with ECM proteins to the cytokine gene expression in human chondrocytes. Human articular chondrocytes expressed VLA-1, -2, -3 and -5 on the cell surface, and could adhere to various ECM proteins, especially to fibronectin (FN). Furthermore, the production of GM-CSF and IL-6 was potently induced by culturing chondrocytes on immobilized FN. This stimulative effect of FN was completely inhibited by an anti-integrin alpha 5 chain mAb, as well as by anti-integrin beta 1 chain mAbs. These results indicate an important role of the VLA-5-mediated interaction with FN in regulating inflammatory cytokine production by human articular chondrocytes.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antibodies, Monoclonal / pharmacology
  • Cartilage, Articular / immunology*
  • Cartilage, Articular / metabolism
  • Cell Adhesion
  • Cells, Cultured
  • Collagen / pharmacology
  • Cytokines / biosynthesis*
  • Extracellular Matrix Proteins / pharmacology
  • Fibronectins / pharmacology*
  • Gene Expression
  • Granulocyte-Macrophage Colony-Stimulating Factor / biosynthesis
  • Humans
  • Integrins / analysis
  • Integrins / biosynthesis*
  • Interleukin-6 / biosynthesis
  • Macromolecular Substances
  • Mice
  • RNA, Messenger / analysis
  • RNA, Messenger / biosynthesis
  • Rats
  • Receptors, Fibronectin / immunology
  • Receptors, Fibronectin / physiology*

Substances

  • Antibodies, Monoclonal
  • Cytokines
  • Extracellular Matrix Proteins
  • Fibronectins
  • Integrins
  • Interleukin-6
  • Macromolecular Substances
  • RNA, Messenger
  • Receptors, Fibronectin
  • Granulocyte-Macrophage Colony-Stimulating Factor
  • Collagen