ArticleJournal of orthopaedic surgery and research2026
STAT1 transcriptionally activates CXCL13 to promote cell inflammation and proliferation and inhibit cell apoptosis in rheumatoid arthritis fibroblast-like synoviocytes.
Article in Journal of orthopaedic surgery and research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Astilbin: a novel therapeutic strategy for bone destruction in rheumatoid arthritis.Frontiers in immunology · 2026Article
- Estrogen and progesterone-mediated differential modulation of CD4Frontiers in immunology · 2026Article
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Authors and funding
6 authors.
Funding
Abstract
backgroundRheumatoid arthritis (RA) is a chronic autoimmune disease characterized by synovial inflammation and joint destruction. C-X-C motif chemokine ligand 13 (CXCL13) is a chemokine involved in B-cell recruitment and lymphoid neogenesis, but its regulatory mechanisms in RA remain unclear.
methodsFibroblast-like synoviocytes (FLS) were isolated from synovial tissues of RA patients and traumatic knee disease volunteers. Differentially expressed genes between healthy and RA synovial tissues were analyzed using GEO datasets (GSE55235, GSE12021, and GSE89408). Quantitative real-time PCR was used to measure mRNA levels of CXCL13, signal transducer and activator of transcription 1 (STAT1), interleukin (IL-6), interleukin-1β (IL-1β), and interleukin-18 (IL-18), while Western blotting was used to detect CXCL13, STAT1, interleukin-8 (IL-8), and cyclooxygenase-2 (COX-2) protein expression. Enzyme-linked immunosorbent assays were used to quantify IL-6, IL-1β, and IL-18 levels. Cell viability, proliferation, and apoptosis were assessed via cell counting kit-8, 5-Ethynyl-2'-deoxyuridine, flow cytometry, and TUNEL assays. Chromatin immunoprecipitation (ChIP) and dual-luciferase reporter assays were used to verify the STAT1-CXCL13 interaction.
resultsCXCL13 and STAT1 were significantly upregulated in RA-FLS. Silencing CXCL13 suppressed pro-inflammatory cytokines (IL-6, IL-1β, IL-18) and proteins (IL-8, COX-2), inhibited cell viability and proliferation, and induced apoptosis. STAT1 knockdown reduced CXCL13 expression with inhibiting phosphorylated STAT1 expression. STAT1 acted as a transcriptional activator of CXCL13 in RA-FLS. Overexpressing CXCL13 reversed the anti-inflammatory, anti-proliferative, and pro-apoptotic effects of STAT1 knockdown in RA-FLS.
conclusionSTAT1 transcriptionally activated CXCL13 to enhance inflammation, promote proliferation, and suppress apoptosis in RA-FLS. These findings highlight the STAT1/CXCL13 axis as a potential therapeutic target for modulating synovial hyperplasia and inflammation in RA.
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