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

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...

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Main Authors: Qing-Zhu Kong, Li-Tao Guo, Jia-Ning Yang, Yan-Fei Wang, Jing-Xin Zhao, Su-Hong Kong, Meng Zhang, Shi Yan, Yu Jin
Format: Article
Language:English
Published: Wiley 2016-01-01
Series:Mediators of Inflammation
Online Access:http://dx.doi.org/10.1155/2016/3906108
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author Qing-Zhu Kong
Li-Tao Guo
Jia-Ning Yang
Yan-Fei Wang
Jing-Xin Zhao
Su-Hong Kong
Meng Zhang
Shi Yan
Yu Jin
author_facet Qing-Zhu Kong
Li-Tao Guo
Jia-Ning Yang
Yan-Fei Wang
Jing-Xin Zhao
Su-Hong Kong
Meng Zhang
Shi Yan
Yu Jin
author_sort Qing-Zhu Kong
collection DOAJ
description 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.
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institution Kabale University
issn 0962-9351
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language English
publishDate 2016-01-01
publisher Wiley
record_format Article
series Mediators of Inflammation
spelling doaj-art-7220fc90e8814e048e036d82d8ddedb02025-08-20T03:33:43ZengWileyMediators of Inflammation0962-93511466-18612016-01-01201610.1155/2016/39061083906108Anti-Inflammatory Effects of TRAF-Interacting Protein in Rheumatoid Arthritis Fibroblast-Like SynoviocytesQing-Zhu Kong0Li-Tao Guo1Jia-Ning Yang2Yan-Fei Wang3Jing-Xin Zhao4Su-Hong Kong5Meng Zhang6Shi Yan7Yu Jin8Department of Orthopedic Trauma, Affiliated Hospital of Chengde Medical University, Chengde, Hebei 06700, ChinaDepartment of Ophthalmology, Affiliated Hospital of Chengde Medical University, Chengde, Hebei 06700, ChinaDepartment of Spinal Surgery, Affiliated Hospital of Chengde Medical University, Chengde, Hebei 06700, ChinaDepartment of Emergency, Affiliated Hospital of Chengde Medical University, Chengde, Hebei 06700, ChinaDepartment of Orthopedic Trauma, Affiliated Hospital of Chengde Medical University, Chengde, Hebei 06700, ChinaDepartment of Gynaecology and Obstetrics, Maternal and Child Health Care Hospital of Longhua County, Chengde, Hebei 068150, ChinaDepartment of Emergency, Affiliated Hospital of Chengde Medical University, Chengde, Hebei 06700, ChinaDepartment of Orthopedic Trauma, Affiliated Hospital of Chengde Medical University, Chengde, Hebei 06700, ChinaDepartment of Orthopedic Trauma, Affiliated Hospital of Chengde Medical University, Chengde, Hebei 06700, ChinaRheumatoid 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.http://dx.doi.org/10.1155/2016/3906108
spellingShingle Qing-Zhu Kong
Li-Tao Guo
Jia-Ning Yang
Yan-Fei Wang
Jing-Xin Zhao
Su-Hong Kong
Meng Zhang
Shi Yan
Yu Jin
Anti-Inflammatory Effects of TRAF-Interacting Protein in Rheumatoid Arthritis Fibroblast-Like Synoviocytes
Mediators of Inflammation
title Anti-Inflammatory Effects of TRAF-Interacting Protein in Rheumatoid Arthritis Fibroblast-Like Synoviocytes
title_full Anti-Inflammatory Effects of TRAF-Interacting Protein in Rheumatoid Arthritis Fibroblast-Like Synoviocytes
title_fullStr Anti-Inflammatory Effects of TRAF-Interacting Protein in Rheumatoid Arthritis Fibroblast-Like Synoviocytes
title_full_unstemmed Anti-Inflammatory Effects of TRAF-Interacting Protein in Rheumatoid Arthritis Fibroblast-Like Synoviocytes
title_short Anti-Inflammatory Effects of TRAF-Interacting Protein in Rheumatoid Arthritis Fibroblast-Like Synoviocytes
title_sort anti inflammatory effects of traf interacting protein in rheumatoid arthritis fibroblast like synoviocytes
url http://dx.doi.org/10.1155/2016/3906108
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