The superficial layer of human articular cartilage is more susceptible to interleukin-1-induced damage than the deeper layers

Arthritis Rheum. 1996 Mar;39(3):478-88. doi: 10.1002/art.1780390316.

Abstract

Objective: To compare the responses of chondrocytes from superficial and deep layers of normal human articular cartilage to interleukin-1 (IL-1) and IL-1 receptor antagonist protein (IRAP), and to evaluate the binding sites for IL-1 on these cells.

Methods: Cartilage and chondrocytes from superficial and deeper layers of human femoral condyles were cultured with and without IL-1 in the presence and absence of IRAP. The effect of these agents on 35S- proteoglycan synthesis and catabolism and production of stromelysin and tissue inhibitor of metalloproteinases 1 (TIMP-1) were measured by biochemical and immunologic assays. Receptor binding was evaluated using 125I-labeled IL-1.

Results: IL-1 induced more severe inhibition of proteoglycan synthesis and a lower ratio of secreted TIMP-l:stromelysin in chondrocytes from superficial cartilage than those from deeper cartilage. IRAP blocked responses to IL-1 more effectively in chondrocytes from deep cartilage than those from superficial cartilage. Chondrocytes from the articular surface showed approximately twice the number of high-affinity b!nding sites for IL-1 as did cells from deep cartilage.

Conclusion: Chondrocytes from the surface of articular cartilage show a greater vulnerability to the harmful effects of IL-1 and are less responsive to the potential therapeutic effects of IRAP than cells in the deeper layers of the tissue.

Publication types

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

MeSH terms

  • Adolescent
  • Adult
  • Cartilage, Articular / cytology
  • Cartilage, Articular / immunology*
  • Cartilage, Articular / ultrastructure
  • Humans
  • Interleukin 1 Receptor Antagonist Protein
  • Interleukin-1 / immunology
  • Interleukin-1 / pharmacology*
  • Middle Aged
  • Proteoglycans / biosynthesis
  • Receptors, Interleukin-1 / antagonists & inhibitors
  • Receptors, Interleukin-1 / immunology
  • Receptors, Interleukin-1 / metabolism
  • Recombinant Proteins / pharmacology
  • Sialoglycoproteins / pharmacology

Substances

  • IL1RN protein, human
  • Interleukin 1 Receptor Antagonist Protein
  • Interleukin-1
  • Proteoglycans
  • Receptors, Interleukin-1
  • Recombinant Proteins
  • Sialoglycoproteins