文献类型：期刊文献

英文题名：TRIM32 promotes inflammatory responses in rheumatoid arthritis fibroblast-like synoviocytes

作者：Liang, Tian[1];Song, Min[1];Xu, Kewu[2];Guo, Chenglong[2];Xu, Hongbin[2];Zhang, Hongwei[2];Xu, Lanping[3]

第一作者：梁恬

通信作者：Xu, LP[1]

机构：[1]Gansu Tradit Chinese Med Univ, Dept Orthoped, Lanzhou, Peoples R China;[2]Gansu Tradit Chinese Med Univ, Affiliated Hosp, Dept Orthoped, Lanzhou, Peoples R China;[3]Gansu Tradit Chinese Med Univ, Affiliated Hosp, Dept Dermatol, Lanzhou, Peoples R China

第一机构：甘肃中医药大学

通信机构：[1]corresponding author), Gansu Tradit Chinese Med Univ, Affiliated Hosp, Dept Dermatol, Lanzhou, Peoples R China.|[10735b845793de6ae2b30]甘肃中医药大学第二附属医院;[10735]甘肃中医药大学;

年份：2020

卷号：91

期号：6

外文期刊名：SCANDINAVIAN JOURNAL OF IMMUNOLOGY

收录：;Scopus(收录号：2-s2.0-85082704963);WOS:【SCI-EXPANDED(收录号:WOS:000520761800001)】；

语种：英文

外文关键词：NF-kappa B; rheumatoid arthritis; TRAF2; TRIM32

摘要：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-alpha) 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 kappa B (NF-kappa 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.