Dispensable role of myeloid differentiation primary response gene 88 (MyD88) and MyD88-dependent toll-like receptors (TLRs) in a murine model of osteoarthritis.

Détails

ID Serval
serval:BIB_6378F9B8886E
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Dispensable role of myeloid differentiation primary response gene 88 (MyD88) and MyD88-dependent toll-like receptors (TLRs) in a murine model of osteoarthritis.
Périodique
Joint, Bone, Spine : Revue du Rhumatisme
Auteur(s)
Nasi S., Ea H.K., Chobaz V., van Lent P., Lioté F., So A., Busso N.
ISSN
1778-7254 (Electronic)
ISSN-L
1297-319X
Statut éditorial
Publié
Date de publication
07/2014
Volume
81
Numéro
4
Pages
320-324
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't Publication Status: ppublish
Résumé
OBJECTIVES: The aim of our study was to evaluate the role of cell-membrane expressed TLRs and the signaling molecule MyD88 in a murine model of OA induced by knee menisectomy (surgical partial removal of the medial meniscus [MNX]).
METHODS: OA was induced in 8-10weeks old C57Bl/6 wild-type (WT) female (n=7) mice and in knockout (KO) TLR-1 (n=7), -2 (n=8), -4 (n=9) -6 (n=5), MyD88 (n=8) mice by medial menisectomy, using the sham-operated contralateral knee as a control. Cartilage destruction and synovial inflammation were evaluated by knee joint histology using the OARSI scoring method. Apoptotic chondrocytes and cartilage metabolism (collagen II synthesis and MMP-mediated aggrecan degradation) were analyzed using immunohistochemistry.
RESULTS: Operated knees exhibited OA features at 8weeks post-surgery compared to sham-operated ones. In menisectomized TLR-1, -2, -4, and -6 deficient mice, cartilage lesions, synovial inflammation and cartilage metabolism were similar to that in operated WT mice. Accordingly, using the same approach, we found no significant protection in MyD88-deficient mice in terms of OA progression as compared to WT littermates.
CONCLUSIONS: Deficiency of TLRs or their signalling molecule MyD88 did not impact on the severity of experimental OA. Our results demonstrate that MyD88-dependent TLRs are not involved in this murine OA model. Moreover, the dispensable role of MyD88, which is also an adaptor for IL-1 receptor signaling, suggests that IL-1 is not a key mediator in the development of OA. This latter hypothesis is strengthened by the lack of efficiency of IL-1β antagonist in the treatment of OA.
Mots-clé
Animals, Cartilage/metabolism, Disease Models, Animal, Female, Immunity, Innate/genetics, Interleukin-1/physiology, Joint Instability/complications, Mice, Mice, Knockout, Myeloid Differentiation Factor 88/metabolism, Osteoarthritis, Knee/etiology, Osteoarthritis, Knee/metabolism, Signal Transduction, Toll-Like Receptors/metabolism
Pubmed
Web of science
Création de la notice
31/12/2014 15:37
Dernière modification de la notice
20/08/2019 15:20
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