ArticleThe Kaohsiung journal of medical sciences2025
RNA Binding Protein YTHDF2 Inhibits Synovial Fibroblast Inflammation and Bone Injury in Rheumatoid Arthritis by Reducing the mRNA Stability of IL-6R.
Article in The Kaohsiung journal of medical sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Metabolic control of RNA methylation in rheumatoid arthritis: from synovial stress to pathogenic cellular adaptation.Frontiers in immunology · 2026Review
- The PANoptotic mosaic of rheumatoid arthritis: epitranscriptomic regulation, systemic relays, and precision death-mode editing.Frontiers in immunology · 2026Review
- RNA Binding Protein YTHDF2 Inhibits Synovial Fibroblast Inflammation and Bone Injury in Rheumatoid Arthritis by Reducing the mRNA Stability of IL-6R.The Kaohsiung journal of medical sciences · 2025Article
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10 authors.
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Abstract
This study examined YTHDF2's role in modulating IL-6R signaling to regulate synovial fibroblast inflammation and bone damage in rheumatoid arthritis (RA). Synovial tissues of RA patients were collected. Human fibroblast-like synoviocyte (FLS), MH7A cell line, was induced with TNF-α and transfected. Cell proliferation was assessed using MTT and EdU assays; apoptosis was measured with flow cytometry, and migration and invasion were evaluated through scratch and Transwell assays. Lentiviral vectors designed to overexpress YTHDF2 or IL-6R were created to study their effects in mice with collagen-induced arthritis (CIA). Pathological changes of ankle joints in mice were observed, and TNF-α, IL-1β, and IL-6 contents were determined. MMP3 and MMP9 levels were detected by Western blot, while YTHDF2 and IL-6R were detected by RT-qPCR and Western blot. The binding relationship between YTHDF2 and IL-6R was studied. YTHDF2 in synovial tissues of RA patients was down-regulated. Elevating YTHDF2 inhibited TNF-α-induced MH7A cell proliferation, migration, invasion, and pro-inflammatory factors; Knocking down YTHDF2 showed the opposite effect. Upregulating YTHDF2 improved synovial inflammation and bone damage in CIA mice. IL-6R in synovial tissues of patients was significantly up-regulated and negatively correlated with YTHDF2 expression. YTHDF2 reduced IL-6R mRNA stability in a m6A-dependent manner. Overexpressing IL-6R impaired the anti-proliferating and anti-inflammatory effect of YTHDF2 on TNF-α-induced MH7A cells. In CIA mice, overexpression of IL-6R reversed the benefits on synovial inflammation and bone injury mediated by up-regulating YTHDF2. YTHDF2 inhibits inflammation and bone damage in RA synovial fibroblasts by reducing the mRNA stability of IL-6R.
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