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TRIM32 promotes inflammatory responses in rheumatoid arthritis fibroblast‐like synoviocytes
Author(s) -
Liang Tian,
Song Min,
Xu Kewu,
Guo Chenglong,
Xu Hongbin,
Zhang Hongwei,
Xu Lanping
Publication year - 2020
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/sji.12876
Subject(s) - ubiquitin ligase , rheumatoid arthritis , ubiquitin , tumor necrosis factor alpha , gene silencing , medicine , cancer research , traf2 , arthritis , osteoarthritis , immunology , receptor , inflammation , chemistry , gene , tumor necrosis factor receptor , pathology , biochemistry , alternative medicine
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.