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.

中文翻译：

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TRIM32促进类风湿关节炎成纤维细胞样滑膜细胞的炎症反应。

类风湿关节炎（RA）是一种全球性自身免疫性疾病。对其病因和作用机理的研究一直是医学界的研究热点。本研究旨在研究E3泛素连接酶三重基序蛋白32（TRIM32）在类风湿关节炎（RA）中的作用。我们发现在RA患者的成纤维样滑膜细胞（FLS）中，TRIM32的表达与其在骨关节炎（OA）患者FLS中的表达相比明显增加。发现广泛使用的促炎性刺激肿瘤坏死因子-α（TNF-α）以时间依赖的方式促进TRIM32表达。此外，我们观察到，TRIM32的过表达加重了FLS中促炎细胞因子的产生，TRIM32的沉默显示了一致的结果。此外，发现TRIM32激活核因子κB（NF-κB）信号传导途径，并且TRIM32可以与TNF受体相关因子2（TRAF2）相互作用，促进RA-FLS中TRAF2的K63连接多聚泛素化。总之，我们建议TRIM32作为RA-FLS中炎症反应的正调节剂。