Production of serum amyloid A in equine articular chondrocytes and fibroblast-like synoviocytes treated with proinflammatory cytokines and its effects on the two cell types in culture

• Stine ^[1] ; Søren ^[2] ; Lise ^[3]
  1. [1] Jacobsen
  2. [2] Ladefoged
  3. [3] C. Berg

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• Localización: American Journal of Veterinary Research, ISSN-e 1943-5681, ISSN 0002-9645, Vol. 77, Nº. 1, 2016, pág. 50
• Idioma: inglés
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  • Production of serum amyloid A in equine articular chondrocytes and fibroblast-like synoviocytes treated with proinflammatory cytokines and its effects on the two cell types in culture Stine Jacobsen, DVM, PhD; Søren Ladefoged, DVM; Lise C. Berg, DVM, PhD Departments of Large Animal Sciences Faculty of Health and Medical Sciences, University of Copenhagen, Højbakkegård Allé 5, DK-2630 Taastrup, Denmark. (Jacobsen, Ladefoged); Animal and Veterinary Basic Sciences Faculty of Health and Medical Sciences, University of Copenhagen, Højbakkegård Allé 5, DK-2630 Taastrup, Denmark. (Berg) Dr. Berg's present address is Department of Large Animal Sciences, University of Copenhagen, Højbakkegård Allé 5, DK-2630 Taastrup, Denmark.

    Address correspondence to Dr. Berg (lcb@sund.ku.dk).

    OBJECTIVE To investigate the role of the major equine acute phase protein serum amyloid A (SAA) in inflammation of equine intraarticular tissues.

    SAMPLE Articular chondrocytes and fibroblast-like synoviocytes (FLSs) from 8 horses (4 horses/cell type).

    PROCEDURES Chondrocytes and FLSs were stimulated in vitro for various periods up to 48 hours with cytokines (recombinant interleukin [IL]-1β, IL-6, tumor necrosis factor-α, or a combination of all 3 [IIT]) or with recombinant SAA. Gene expression of SAA, IL-6, matrix metalloproteinases (MMP)-1 and −3, and cartilage-derived retinoic acid-sensitive protein were assessed by quantitative real-time PCR assay; SAA protein was evaluated by immunoturbidimetry and denaturing isoelectric focusing and western blotting.

    RESULTS All cytokine stimulation protocols increased expression of SAA mRNA and resulted in detectable SAA protein production in chondrocytes and FLSs. Isoforms of SAA in lysed chondrocytes and their culture medium corresponded to those previously detected in synovial fluid from horses with joint disease. When exposed to SAA, chondrocytes and FLSs had increased expression of IL-6, SAA, and MMP3, and chondrocytes had increased expression of MMP-1. Chondrocytes had decreased expression of cartilage-derived retinoic acid-sensitive protein.

    CONCLUSIONS AND CLINICAL RELEVANCE Upregulation of SAA in chondrocytes and FLSs stimulated with proinflammatory cytokines and the proinflammatory effects of SAA suggested that SAA may be involved in key aspects of pathogenesis of the joint inflammation in horses.

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