Drogi użytkowniku, aplikacja do prawidłowego działania wymaga obsługi JavaScript. Proszę włącz obsługę JavaScript w Twojej przeglądarce.

Przeglądasz jako GOŚĆ
Tytuł pozycji:

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

Tytuł :
TRIM32 promotes inflammatory responses in rheumatoid arthritis fibroblast-like synoviocytes.
Autorzy :
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.
Pokaż więcej
Źródło :
Scandinavian journal of immunology [Scand J Immunol] 2020 Jun; Vol. 91 (6), pp. e12876. Date of Electronic Publication: 2020 Mar 20.
Typ publikacji :
Journal Article
Język :
Imprint Name(s) :
Publication: Oxford : Blackwell Scientific Publications
Original Publication: Oslo, Universitetsforlaget.
MeSH Terms :
Arthritis, Rheumatoid/*metabolism
Transcription Factors/*metabolism
Tripartite Motif Proteins/*metabolism
Ubiquitin-Protein Ligases/*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
References :
Kugyelka R, Kohl Z, Olasz K, et al. Enigma of IL-17 and Th17 cells in rheumatoid arthritis and in autoimmune animal models of arthritis. Mediat Inflamm. 2016;2016:6145810.
Chen Y, Xian P-F, Yang L, Wang S-X. MicroRNA-21 promotes proliferation of fibroblast-like synoviocytes through mediation of NF-κB nuclear translocation in a rat model of collagen-induced rheumatoid arthritis. BioMed Res Int. 2016;2016:9279078.
Zhou L, Li L, Wang Y, Gao Q, Geng Y-Q. Effects of RANKL on the proliferation and apoptosis of fibroblast-like synoviocytes in rheumatoid arthritis through regulating the NF-κB signaling pathway. Eur Rev Med Pharmacol Sci. 2019;23:9215-9221.
Lu X, Qian J. Downregulated MEG3 participates in rheumatoid arthritis via promoting proliferation of fibroblast-like synoviocytes. Exp Ther Med. 2019;17:1637-1642.
Lin Y, Luo Z. NLRP6 facilitates the interaction between TAB2/3 and TRIM38 in rheumatoid arthritis fibroblast-like synoviocytes. FEBS Lett. 2017;591:1141-1149.
Sardiello M, Cairo S, Fontanella B, Ballabio A, Meroni G. Genomic analysis of the TRIM family reveals two groups of genes with distinct evolutionary properties. BMC Evol Biol. 2008;8:225.
Pan S, Deng Y, Fu J, et al. TRIM52 promotes colorectal cancer cell proliferation through the STAT3 signaling. Cancer Cell Int. 2019;19:57.
Huang Q, Zhu X, Xu M. Silencing of TRIM10 alleviates apoptosis in cellular model of Parkinson’s disease. Biochem Biophys Res Commun. 2019;518:451-458.
Sparrer KMJ, Gack MU. TRIM proteins: New players in virus-induced autophagy. PLoS Pathog. 2018;14:e1006787.
Ozato K, Shin D-M, Chang T-H, Morse HC. TRIM family proteins and their emerging roles in innate immunity. Nat Rev Immunol. 2008;8:849-860.
Cambiaghi V, Giuliani V, Lombardi S, Marinelli C, Toffalorio F, Pelicci PG. TRIM proteins in cancer. Adv Exp Med Biol. 2012;770:77-91.
Meroni G, Diez-Roux G. TRIM/RBCC, a novel class of “single protein RING finger” E3 ubiquitin ligases. BioEssays. 2005;27:1147-1157.
Kano S, Miyajima N, Fukuda S, Hatakeyama S. Tripartite motif protein 32 facilitates cell growth and migration via degradation of Abl-interactor 2. Cancer Res. 2008;68:5572-5580.
Zhang J, Hu M-M, Wang Y-Y, Shu H-B. TRIM32 protein modulates type I interferon induction and cellular antiviral response by targeting MITA/STING protein for K63-linked ubiquitination. J Biol Chem. 2012;287:28646-28655.
Nicklas S, Otto A, Wu X, et al. TRIM32 regulates skeletal muscle stem cell differentiation and is necessary for normal adult muscle regeneration. PLoS one. 2012;7:e30445.
Mokhonova EI, Avliyakulov NK, Kramerova I, Kudryashova E, Haykinson MJ, Spencer MJ. The E3 ubiquitin ligase TRIM32 regulates myoblast proliferation by controlling turnover of NDRG2. Hum Mol Genet. 2015;24:2873-2883.
Livak KJ, Schmittgen TD. Analysis of relative gene expression data using real-time quantitative PCR and the 2−ΔΔCT method. Methods. 2001;25:402-408.
Kong Q-Z, Guo L-T, Yang J-N, et al. Anti-inflammatory effects of TRAF-interacting protein in rheumatoid arthritis fibroblast-like synoviocytes. Mediat Inflamm. 2016;2016:1-9.
Wang C, Xu J, Fu H, et al. TRIM32 promotes cell proliferation and invasion by activating β-catenin signalling in gastric cancer. J Cell Mol Med. 2018;22:5020-5028.
Dreyer L, Mellemkjaer L, Andersen AR, et al. Incidences of overall and site specific cancers in TNFα inhibitor treated patients with rheumatoid arthritis and other arthritides - a follow-up study from the DANBIO Registry. Ann Rheum Dis. 2013;72:79-82.
Roman-Blas JA, Jimenez SA. NF-κB as a potential therapeutic target in osteoarthritis and rheumatoid arthritis. Osteoarthr Cartilage. 2006;14:839-848.
di Rienzo M, Antonioli M, Fusco C, et al. Autophagy induction in atrophic muscle cells requires ULK1 activation by TRIM32 through unanchored K63-linked polyubiquitin chains. Sci Adv. 2019;5:eaau8857.
Wang L, Liu Y, Su X, Liu S. Effect of etanercept, infliximab and methotrexate in the treatment of arthritis. Drug Res. 2015;65:96-100.
Ma Z, Wang B, Wang M, et al. TL1A increased IL-6 production on fibroblast-like synoviocytes by preferentially activating TNF receptor 2 in rheumatoid arthritis. Cytokine. 2016;83:92-98.
Simmonds RE, Foxwell BM. Signalling, inflammation and arthritis: NF-kappaB and its relevance to arthritis and inflammation. Rheumatology. 2008;47:584-590.
Doss HM, Ganesan R, Rasool M. Trikatu, an herbal compound ameliorates rheumatoid arthritis by the suppression of inflammatory immune responses in rats with adjuvant-induced arthritis and on cultured fibroblast like synoviocytes via the inhibition of the NFκB signaling pathway. Chem Biol Interact. 2016;258:175-186.
Qiang J, Lv T, Wu Z, Yang X. Down-regulation of microRNA-142-3p inhibits the aggressive phenotypes of rheumatoid arthritis fibroblast-like synoviocytes through inhibiting nuclear factor-κB signaling. Biosci Rep. 2019;39(7). pii: BSR20190700.
Zhang L-M, Zhou J-J, Luo C-L. CYLD suppression enhances the pro-inflammatory effects and hyperproliferation of rheumatoid arthritis fibroblast-like synoviocytes by enhancing NF-κB activation. Arthritis Res Ther. 2018;20:219.
Fan Y, Yu Y, Shi Y, et al. Lysine 63-linked polyubiquitination of TAK1 at lysine 158 is required for tumor necrosis factor alpha- and interleukin-1beta-induced IKK/NF-kappaB and JNK/AP-1 activation. J Biol Chem. 2010;285:5347-5360.
Contributed Indexing :
Keywords: NF-κB; TRAF2; TRIM32; rheumatoid arthritis
Substance Nomenclature :
0 (Cytokines)
0 (Inflammation Mediators)
0 (NF-kappa B)
0 (TNF Receptor-Associated Factor 2)
0 (Transcription Factors)
0 (Tripartite Motif Proteins)
EC (TRIM32 protein, human)
EC (Ubiquitin-Protein Ligases)
Entry Date(s) :
Date Created: 20200308 Date Completed: 20200608 Latest Revision: 20200608
Update Code :
Czasopismo naukowe
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.)

Ta witryna wykorzystuje pliki cookies do przechowywania informacji na Twoim komputerze. Pliki cookies stosujemy w celu świadczenia usług na najwyższym poziomie, w tym w sposób dostosowany do indywidualnych potrzeb. Korzystanie z witryny bez zmiany ustawień dotyczących cookies oznacza, że będą one zamieszczane w Twoim komputerze. W każdym momencie możesz dokonać zmiany ustawień dotyczących cookies