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The British veterinary journal1992; 148(5); 389-397; doi: 10.1016/0007-1935(92)90026-W

Equine chondrocyte activation by a variety of stimuli.

Abstract: There is increasing evidence that the chondrocyte is capable of considerable anabolic and catabolic activity. In the case of equine chondrocytes, this study demonstrates that a variety of factors involved in the pathogenesis of joint disease stimulate the production of prostaglandin E2. These include exposure to IL-1, bone fragments and LPS. In addition, an IL-1-like factor was shown to be produced by the chondrocyte itself, when stimulated by LPS, providing a possible mechanism for amplification of extra-cartilagenous signals and even autocrine control. Considered together with evidence of increased synthesis of proteoglycan molecules by chondrocytes in diseased cartilage, this offers the exciting possibility of development of therapeutic agents to assist cartilage repair.
Publication Date: 1992-09-01 PubMed ID: 1422781DOI: 10.1016/0007-1935(92)90026-WGoogle Scholar: Lookup
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  • Journal Article
  • Research Support
  • Non-U.S. Gov't

Summary

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This study unravels that various factors responsible for joint disease stimulate the production of prostaglandin E2, a lipid compound having hormone-like effects, in horse cartilage cells. It highlights the potential for developing treatment options that can aid cartilage repair.

Background

  • The research focuses on chondrocytes, which are cells found in healthy cartilage responsible for maintaining it. They have a dual nature, with a capacity for notable anabolic (constructive metabolism) and catabolic (destructive metabolism) activity.

Findings

  • The study indicates that certain factors involved in the onset and progression of joint disease stimulate equine chondrocytes leading to the production of prostaglandin E2, a substance that plays a pivotal role in inflammation.
  • These factors include Interleukin-1 (IL-1), bone fragments, and lipopolysaccharides (LPS).
  • The study makes an important observation that an IL-1-like factor is produced by the chondrocyte itself when triggered by LPS. This suggests a possible mechanism for boosting extra-cartilaginous signals and perhaps even autocrine control, where cells respond to signals they themselves generate.

Implications

  • When viewed together with evidence of elevated synthesis of proteoglycan molecules (essential for the structural integrity of the cartilage) by chondrocytes in diseased cartilage, the study opens up intriguing prospects for possible treatments targeting cartilage repair.

Conclusion

  • In essence, the research provides valuable insights into the how various factors involved in joint disease potentially stimulate pathophysiological responses in equine cartilage cells. The findings advance our knowledge in the field, spotlighting potential targets for therapeutic intervention in cartilage repair.

Cite This Article

APA
May SA, Hooke RE, Lees P. (1992). Equine chondrocyte activation by a variety of stimuli. Br Vet J, 148(5), 389-397. https://doi.org/10.1016/0007-1935(92)90026-W

Publication

ISSN: 0007-1935
NlmUniqueID: 0372554
Country: England
Language: English
Volume: 148
Issue: 5
Pages: 389-397

Researcher Affiliations

May, S A
  • Department of Veterinary Basic Sciences, Royal Veterinary College, North Mymms, Hatfield, Herts.
Hooke, R E
    Lees, P

      MeSH Terms

      • Animals
      • Bone and Bones / physiology
      • Cartilage, Articular / cytology
      • Cells, Cultured
      • Dinoprostone / biosynthesis
      • Horse Diseases / etiology
      • Horses
      • Interleukin-1 / physiology
      • Lipopolysaccharides / metabolism
      • Osteoarthritis / etiology
      • Osteoarthritis / veterinary

      Citations

      This article has been cited 1 times.
      1. Smit Y, Marais HJ, Thompson PN, Mahne AT, Goddard A. Clinical findings, synovial fluid cytology and growth factor concentrations after intra-articular use of a platelet-rich product in horses with osteoarthritis. J S Afr Vet Assoc 2019 May 23;90(0):e1-e9.
        doi: 10.4102/jsava.v90i0.1721pubmed: 31170778google scholar: lookup