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Mediators of Inflammation
Volume 2016, Article ID 3906108, 9 pages
http://dx.doi.org/10.1155/2016/3906108
Research Article

Anti-Inflammatory Effects of TRAF-Interacting Protein in Rheumatoid Arthritis Fibroblast-Like Synoviocytes

1Department of Orthopedic Trauma, Affiliated Hospital of Chengde Medical University, Chengde, Hebei 06700, China
2Department of Ophthalmology, Affiliated Hospital of Chengde Medical University, Chengde, Hebei 06700, China
3Department of Spinal Surgery, Affiliated Hospital of Chengde Medical University, Chengde, Hebei 06700, China
4Department of Emergency, Affiliated Hospital of Chengde Medical University, Chengde, Hebei 06700, China
5Department of Gynaecology and Obstetrics, Maternal and Child Health Care Hospital of Longhua County, Chengde, Hebei 068150, China

Received 27 April 2016; Accepted 4 October 2016

Academic Editor: Luca Cantarini

Copyright © 2016 Qing-Zhu Kong et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Rheumatoid arthritis (RA) is a chronic systemic inflammatory disease characterized by inflammatory cell infiltration, synovial inflammation, and cartilage destruction. Proliferative fibroblast-like synoviocytes (FLS) play crucial roles in both propagation of inflammation and joint damage because of their production of great amount of proinflammatory cytokines and proteolytic enzymes. In this study, we investigate the role of TRAF-interacting protein (TRIP) in regulating inflammatory process in RA-FLS. TRIP expression was attenuated in RA-FLS compared with osteoarthritis- (OA-) FLS. Overexpression of TRIP significantly inhibited the activation of NF-κB signaling and decreased the production of proinflammatory cytokines and matrix metalloproteinases (MMPs) in TNFα-stimulated RA-FLS. Furthermore, TRIP was found to interact with transforming growth factor β-activated kinase 1 (TAK1) and promoting K48-linked polyubiquitination of TAK1 in RA-FLS. Our results demonstrate that TRIP has anti-inflammatory effects on RA-FLS and suggest TRIP as a potential therapeutic target for human RA.