Chondrocyte phenotyping in human osteoarthritis

Clin Rheumatol. 1998;17(2):99-104. doi: 10.1007/BF01452253.

Abstract

Cell-ECM (extracellular matrix) interactions are believed to play a key role in maintaining the normal structure of tissues such as cartilage. Cell surface adhesion molecules have been reported to mediate chondrocyte binding to ECM proteins in human normal cartilage but the behaviour of these molecules in human osteoarthritic cartilage is unknown. We studied receptor matrix proteins on freshly isolated chondrocytes obtained from 10 patients with osteoarthritis (OA). Chondrocytes were isolated by enzymatic digestion from three zones of the articular cartilage with a different degree of macroscopic and microscopic damage and chondrocyte phenotype was defined by flow cytometry. Chondrocytes strongly expressed beta1, integrin but not beta3 integrin. LFA-1 (CD18/CD11a) and ICAM-1 (CD54) antigens were almost undetectable. Interestingly, beta1 expression was significantly higher in the minimally damaged zone than in the zones with medium and maximum damage. These data show that beta1-integrin-mediated chondrocyte-ECM interactions decrease in osteoarthritic cartilage suggesting that perturbations of chondrocyte-matrix signalling occurs during OA.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aged
  • Cell Cycle
  • Cells, Cultured
  • Chondrocytes / metabolism*
  • Chondrocytes / pathology
  • Female
  • Flow Cytometry
  • Humans
  • Integrins / metabolism
  • Intercellular Adhesion Molecule-1 / metabolism
  • Lymphocyte Function-Associated Antigen-1 / metabolism
  • Male
  • Membrane Proteins / metabolism*
  • Middle Aged
  • Osteoarthritis / metabolism*
  • Osteoarthritis / pathology
  • Phenotype

Substances

  • Integrins
  • Lymphocyte Function-Associated Antigen-1
  • Membrane Proteins
  • Intercellular Adhesion Molecule-1