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Time-dependent changes in gene expression induced in vitro by interleukin-1 beta in equine articular cartilage

Artikel i vetenskaplig tidskrift
Författare M. Lofgren
Emilia Svala
Anders Lindahl
Eva Skiöldebrand
S. Ekman
Publicerad i Research in Veterinary Science
Volym 118
Sidor 466-476
ISSN 0034-5288
Publiceringsår 2018
Publicerad vid Institutionen för biomedicin, avdelningen för klinisk kemi och transfusionsmedicin
Sidor 466-476
Språk en
Länkar https://doi.org/10.1016/j.rvsc.2018...
Ämnesord Osteoarthritis, Inflammation, Extracellular matrix, Chondrocyte, chondrocyte differentiation pathway, ii collagen gene, rheumatoid-arthritis, pericellular matrix, candidate genes, osteoarthritis, perlecan, sox9, proteoglycan, notch, Veterinary Sciences
Ämneskategorier Veterinärmedicin

Sammanfattning

Osteoarthritis is an inflammatory and degenerative joint disease commonly affecting horses. To identify genes of relevance for cartilage pathology in osteoarthritis we studied the time-course effects of interleukin (IL)-1 beta on equine articular cartilage. Articular cartilage explants from the distal third metacarpal bone were collected postmortem from three horses without evidence of joint disease. The explants were stimulated with IL-1 beta for 27 days and global gene expression was measured by microarray. Gene expression was compared to that of unstimulated explants at days 3, 9, 15, 21 and 27. Release of inflammatory proteins was measured using Proximity Extension Assay. Stimulation with IL-1 beta led to time-dependent changes in gene expression related to inflammation, the extracellular matrix (ECM), and phenotypic alterations. Gene expression and protein release of cytokines, chemokines, and matrix-degrading enzymes increased in the stimulated explants. Collagen type II was down regulated from day 15, whereas other ECM molecules were downregulated earlier. In contrast molecules involved in ECM signaling (perlecan, chondroitin sulfate proteoglycan 4, and syndecan 4) were upregulated. At the late time points, genes related to a chondrogenic phenotype were downregulated, and genes related to a hypertrophic phenotype were upregulated, suggesting a transition towards hypertrophy later in the culturing period. The data suggest that this in vitro model mimics time course events of in vivo inflammation in OA and it may be valuable as an in vitro tool to test treatments and to study disease mechanisms.

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Denna text är utskriven från följande webbsida:
http://www.gu.se/forskning/publikation/?publicationId=268750
Utskriftsdatum: 2019-08-21