TRIM32 promotes inflammatory responses in rheumatoid arthritis fibroblast-like synoviocytes.

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-?) 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 ?B (NF-?B) 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.
Mesh Terms:
Arthritis, Rheumatoid, Cell Proliferation, Cells, Cultured, Cytokines, Fibroblasts, Humans, Inflammation, Inflammation Mediators, NF-kappa B, Signal Transduction, Synoviocytes, TNF Receptor-Associated Factor 2, Transcription Factors, Tripartite Motif Proteins, Ubiquitin-Protein Ligases, Ubiquitination, Up-Regulation
Scand J Immunol
Date: Jun. 01, 2020
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