ArticleMolecular medicine reports2017
The tripartite motif-containing protein 3 on the proliferation and cytokine secretion of rheumatoid arthritis fibroblast-like synoviocytes.
Article in Molecular medicine reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 21 citations in OpenAlex.
- TRIM proteins as emerging regulators of immune pathways: potential therapeutic targets in immune-related disorders.Frontiers in immunology · 2026Review
- TRIM3 exacerbates chondrocyte apoptosis through suppression of AKT/mTOR signaling pathway in osteoarthritis.Journal of orthopaedic surgery and research · 2025Article
- Research progress on exosomal proteins as diagnostic markers of gastric cancer (review article).Clinical and experimental medicine · 2023Review
- Overexpression of TRIM3 protects against LPS-induced acute kidney injury via repressing IRF3 pathway and NLRP3 inflammasome.International urology and nephrology · 2022Article
- Identification of Tissue-Specific Expressed Hub Genes and Potential Drugs in Rheumatoid Arthritis Using Bioinformatics Analysis.Frontiers in genetics · 2022Article
- Identification of hub genes in rheumatoid arthritis through an integrated bioinformatics approach.Journal of orthopaedic surgery and research · 2021Article
- Ubiquitination of TLR3 by TRIM3 signals its ESCRT-mediated trafficking to the endolysosomes for innate antiviral response.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Inhibition of the TGF-β/Smads signaling pathway attenuates pulmonary fibrosis and induces anti-proliferative effect on synovial fibroblasts in rheumatoid arthritis.International journal of clinical and experimental pathology · 2019Article
- TRIM3 Negatively Regulates Autophagy Through Promoting Degradation of Beclin1 in Ewing Sarcoma Cells.OncoTargets and therapy · 2019Article
- Role of lentivirus-mediated overexpression of SOCS3 in proliferation and apoptosis of fibroblasts-like synoviocytes in Lewis rats with adjuvant-induced rheumatoid arthritis.International journal of clinical and experimental pathology · 2018Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent studies have revealed fibroblast-like synoviocytes (FLS) as a pivotal effector cell in the inflamed joint of rheumatoid arthritis (RA) patients. FLS exhibit high proliferation rates and constitutive expression of cytokines, contributing to the pathogenesis of RA. In this study, we found that the expression of tripartite motif-containing protein 3 (TRIM3), a candidate tumor suppressor gene, was lower in synovial tissue samples of RA patients than in that of healthy controls. We then investigated the role of TRIM3 on the proliferation and cytokine secretion of primary cultured FLS from RA patients. Enforced expression of TRIM3 in RA FLS led to significantly decreased cell proliferation as indicated by Cell Counting Kit-8 assay, reduced secretion of tumor necrosis factor-α (TNF)-α, interleukin (IL)-1β and IL-6 as indicated by enzyme-linked immunosorbent assays, and decreased p38 phosphorylation as assessed by western blot analysis. The proteins promoting cell cycles (cyclin D1 and PCNA) were downregulated and the protein negatively regulating cell cycle progression (p53 and p21) was upregulated after TRIM3 overexpression. Importantly, TRIM3 knockdown had reverse effects on cell proliferation, which was suppressed by the p38-specific inhibitor SB203580. In conclusion, the current results demonstrated the downregulation of TRIM3 expression in RA synovial tissues. Importantly, TRIM3 exerted an anti-proliferation role in RA FLS via p38 signaling pathway.
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