Modulation of the expression of matrix metalloproteinase and tissue inhibitors of metalloproteinases by TGF-beta1 and IGF-1 in primary human articular and bovine nasal chondrocytes stimulated with TNF-alpha

Cytokine. 2001 Oct 7;16(1):31-5. doi: 10.1006/cyto.2001.0950.

Abstract

Tumour necrosis factor-alpha (TNF-alpha) was able to promote collagen breakdown from bovine cartilage in explant culture. This release was dependent upon matrix metalloproteinases (MMPs) and could be prevented by transforming growth factor-beta1 (TGF-beta1) or insulin-like growth factor-1. Both growth factors reduced the expression and secretion of collagenase enzymes, and TGF-beta1 induced tissue inhibitor of metalloproteinase production. This study shows for the first time that these anabolic growth factors can protect cartilage against TNF-alpha-induced destruction.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Blotting, Northern
  • Cartilage, Articular / drug effects*
  • Cartilage, Articular / enzymology
  • Cattle
  • Chondrocytes / drug effects*
  • Chondrocytes / enzymology
  • Collagen / biosynthesis
  • Collagen / genetics
  • Gene Expression
  • Humans
  • Insulin-Like Growth Factor I / pharmacology*
  • Matrix Metalloproteinases / metabolism*
  • Tissue Inhibitor of Metalloproteinases / metabolism*
  • Transforming Growth Factor beta / pharmacology*
  • Transforming Growth Factor beta1
  • Tumor Necrosis Factor-alpha / pharmacology*

Substances

  • TGFB1 protein, human
  • Tissue Inhibitor of Metalloproteinases
  • Transforming Growth Factor beta
  • Transforming Growth Factor beta1
  • Tumor Necrosis Factor-alpha
  • Insulin-Like Growth Factor I
  • Collagen
  • Matrix Metalloproteinases