Growth factor actions on articular cartilage.

Stephen Trippel

Research output: Contribution to journalArticle

215 Citations (Scopus)

Abstract

Polypeptide growth factors play a major role in the regulation of cell behavior, including that of articular chondrocytes. Among the most influential of these factors identified for articular cartilage are insulin like growth factor I (IGF-I), basic fibroblast growth factor (bFGF), and transforming growth factor beta (TGF beta). IGF-I stimulates articular chondrocyte matrix synthetic and mitotic activity and inhibits chondrocyte mediated matrix catabolism. The role of bFGF as a potent mitogen for articular chondrocytes is well established. In contrast, this factor appears to play a complex role in matrix synthesis and degradation, promoting both anabolic and catabolic functions. Both IGF-I and bFGF have been shown to augment articular cartilage repair in vivo. TGF beta is particularly dependent upon the context in which it acts, eliciting seemingly opposite effects under different experimental conditions. These and other factors interact to modulate their respective actions, creating effector cascades and feedback loops of intercellular and intracellular events that control articular chondrocyte functions. Elucidation of the actions and interactions of these factors may be expected to clarify the etiopathogenesis of osteoarthritis and possibly offer novel methods for its treatment.

Original languageEnglish (US)
Pages (from-to)129-132
Number of pages4
JournalThe Journal of rheumatology. Supplement
Volume43
StatePublished - Feb 1995
Externally publishedYes

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Articular Cartilage
Chondrocytes
Intercellular Signaling Peptides and Proteins
Fibroblast Growth Factor 2
Joints
Insulin-Like Growth Factor I
Transforming Growth Factor beta
Mitogens
Osteoarthritis
Peptides

ASJC Scopus subject areas

  • Medicine(all)
  • Immunology
  • Rheumatology

Cite this

Growth factor actions on articular cartilage. / Trippel, Stephen.

In: The Journal of rheumatology. Supplement, Vol. 43, 02.1995, p. 129-132.

Research output: Contribution to journalArticle

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