TRIM32 promotes inflammatory responses in rheumatoid arthritis fibroblast-like synoviocytes.
Liang T; Department of Orthopedics, Gansu Traditional Chinese Medicine University, Lanzhou, China.
Song M; Department of Orthopedics, Gansu Traditional Chinese Medicine University, Lanzhou, China.
Xu K; Department of Orthopedics, Affiliated Hospital of Gansu Traditional Chinese Medicine University, Lanzhou, China.
Guo C; Department of Orthopedics, Affiliated Hospital of Gansu Traditional Chinese Medicine University, Lanzhou, China.
Xu H; Department of Orthopedics, Affiliated Hospital of Gansu Traditional Chinese Medicine University, Lanzhou, China.
Zhang H; Department of Orthopedics, Affiliated Hospital of Gansu Traditional Chinese Medicine University, Lanzhou, China.
Xu L; Department of Dermatology, Affiliated Hospital of Gansu Traditional Chinese Medicine University, Lanzhou, China.
Scandinavian journal of immunology [Scand J Immunol] 2020 Jun; Vol. 91 (6), pp. e12876. Date of Electronic Publication: 2020 Mar 20.
Typ publikacji :
Imprint Name(s) :
Publication: Oxford : Blackwell Scientific Publications
Original Publication: Oslo, Universitetsforlaget.
MeSH Terms :
Tripartite Motif Proteins/*metabolism
Arthritis, Rheumatoid/immunology ; Cell Proliferation ; Cells, Cultured ; Cytokines/metabolism ; Humans ; Inflammation/immunology ; Inflammation Mediators/metabolism ; NF-kappa B/metabolism ; Signal Transduction ; TNF Receptor-Associated Factor 2/metabolism ; Transcription Factors/genetics ; Tripartite Motif Proteins/genetics ; Ubiquitin-Protein Ligases/genetics ; Ubiquitination ; Up-Regulation
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Contributed Indexing :
Keywords: NF-κB; TRAF2; TRIM32; rheumatoid arthritis
Substance Nomenclature :
0 (Inflammation Mediators)
0 (NF-kappa B)
0 (TNF Receptor-Associated Factor 2)
0 (Transcription Factors)
0 (Tripartite Motif Proteins)
EC 18.104.22.168 (TRIM32 protein, human)
EC 22.214.171.124 (Ubiquitin-Protein Ligases)
Entry Date(s) :
Date Created: 20200308 Date Completed: 20200608 Latest Revision: 20200608
Update Code :
Rheumatoid arthritis (RA) is a worldwide autoimmune disease. The study of its aetiology and mechanism has always been a focus topic in medicine. This research was designed to investigate the effect of E3 ubiquitin ligase tripartite motif protein 32 (TRIM32) in rheumatoid arthritis (RA). We found in fibroblast-like synoviocytes (FLS) of RA patients, the expression of TRIM32 was significantly increased compared with its expression in osteoarthritis (OA) patients FLS. A widely used pro-inflammatory stimuli tumour necrosis factor-alpha (TNF-α) was found to promote TRIM32 expression in a time-dependent manner. Furthermore, we observed that overexpression of TRIM32 aggravated the production of pro-inflammatory cytokines in FLS, silencing of TRIM32 showed the consistent results. In addition, TRIM32 was found to activate nuclear factor κB (NF-κB) signalling pathway, and TRIM32 could interact with TNF receptor-associated factor 2 (TRAF2) to promote the K63-linked polyubiquitination of TRAF2 in RA-FLS. In conclusion, we suggested that TRIM32 as a positive regulator of inflammatory responses in RA-FLS.
(© 2020 The Scandinavian Foundation for Immunology.)