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Article

Tumor necrosis factor receptor-associated factor 6 promotes migration of rheumatoid arthritis fibroblast-like synoviocytes

  • Authors:
    • Huiqin Wang
    • Weixia Chen
    • Ling Wang
    • Faxin Li
    • Chunling Zhang
    • Li Xu
  • View Affiliations / Copyright

    Affiliations: Department of Clinical Laboratory, Zaozhuang Municipal Hospital, Zaozhuang, Shandong 277102, P.R. China, Department of Rheumatology, Zaozhuang Municipal Hospital, Zaozhuang, Shandong 277102, P.R. China, Department of Rheumatology, Jinan Central Hospital Affiliated to Shandong University, Jinan, Shandong 250204, P.R. China
  • Pages: 2761-2766
    |
    Published online on: December 17, 2014
       https://doi.org/10.3892/mmr.2014.3104
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Abstract

Fibroblast‑like synoviocytes (FLSs) have a pivotal role in the destruction of joints in rheumatoid arthritis (RA). Tumor necrosis factor receptor‑associated factor 6 (TRAF6) is a critical mediator in the inflammatory pathway and of the activity of osteoclasts. The aim of the present study was to investigate whether TRAF6 is involved in the progression of RA in mouse collagen‑induced arthritis (CIA) and human RA FLSs in vitro. In vivo mouse models were transfected with TRAF6 small interfering (si)RNA (siTRAF6) and TRAF6 inhibition was achieved in FLSs using an anti‑TRAF6 monoclonal antibody in vitro in order to assess the effects of TRAF6 inhibition on the migration and invasion of FLSs. Inhibition of TRAF6 using mouse specific siTRAF6 reduced the severity of arthritis and joint inflammation. Serum anti‑collagen II antibodies, matrix metalloproteinase (MMP)‑1, MMP‑3 and MMP‑9 were also inhibited in CIA mice by siTRAF6. The levels of MMPs produced by IL‑1β‑stimulated human RA‑FLSs were reduced by anti‑TRAF6 monoclonal antibody. TRAF6 blockade significantly suppressed the IL‑1β‑stimulated migration and invasion of human RA‑FLSs. These results support a role for TRAF6 in the pathogenesis of RA, and suggest that the TRAF6 blockade may be a potential strategy in the management of RA.
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Copy and paste a formatted citation
Spandidos Publications style
Wang H, Chen W, Wang L, Li F, Zhang C and Xu L: Tumor necrosis factor receptor-associated factor 6 promotes migration of rheumatoid arthritis fibroblast-like synoviocytes. Mol Med Rep 11: 2761-2766, 2015.
APA
Wang, H., Chen, W., Wang, L., Li, F., Zhang, C., & Xu, L. (2015). Tumor necrosis factor receptor-associated factor 6 promotes migration of rheumatoid arthritis fibroblast-like synoviocytes. Molecular Medicine Reports, 11, 2761-2766. https://doi.org/10.3892/mmr.2014.3104
MLA
Wang, H., Chen, W., Wang, L., Li, F., Zhang, C., Xu, L."Tumor necrosis factor receptor-associated factor 6 promotes migration of rheumatoid arthritis fibroblast-like synoviocytes". Molecular Medicine Reports 11.4 (2015): 2761-2766.
Chicago
Wang, H., Chen, W., Wang, L., Li, F., Zhang, C., Xu, L."Tumor necrosis factor receptor-associated factor 6 promotes migration of rheumatoid arthritis fibroblast-like synoviocytes". Molecular Medicine Reports 11, no. 4 (2015): 2761-2766. https://doi.org/10.3892/mmr.2014.3104
Copy and paste a formatted citation
x
Spandidos Publications style
Wang H, Chen W, Wang L, Li F, Zhang C and Xu L: Tumor necrosis factor receptor-associated factor 6 promotes migration of rheumatoid arthritis fibroblast-like synoviocytes. Mol Med Rep 11: 2761-2766, 2015.
APA
Wang, H., Chen, W., Wang, L., Li, F., Zhang, C., & Xu, L. (2015). Tumor necrosis factor receptor-associated factor 6 promotes migration of rheumatoid arthritis fibroblast-like synoviocytes. Molecular Medicine Reports, 11, 2761-2766. https://doi.org/10.3892/mmr.2014.3104
MLA
Wang, H., Chen, W., Wang, L., Li, F., Zhang, C., Xu, L."Tumor necrosis factor receptor-associated factor 6 promotes migration of rheumatoid arthritis fibroblast-like synoviocytes". Molecular Medicine Reports 11.4 (2015): 2761-2766.
Chicago
Wang, H., Chen, W., Wang, L., Li, F., Zhang, C., Xu, L."Tumor necrosis factor receptor-associated factor 6 promotes migration of rheumatoid arthritis fibroblast-like synoviocytes". Molecular Medicine Reports 11, no. 4 (2015): 2761-2766. https://doi.org/10.3892/mmr.2014.3104
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