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Updated: Jan 17, 2026

An Adoptive Transfer Model of Rheumatoid Arthritis in Mice
Published on: June 6, 2025
BMP9 suppresses TNF-α-induced inflammatory response in fibroblast-like synoviocytes through Smad pathway in
Biao Song1, Dan-Tong Sun1, Yong-Feng Cheng2
1Department of Pharmacy, the First Affiliated Hospital of Anhui Medical University, Hefei 230022, China; Inflammation and Immune Mediated Diseases Laboratory of Anhui Province, Anhui Institute of Innovative Drugs, The Key Laboratory of Anti-inflammatory and Immune Medicines, Ministry of Education, School of Pharmacy, Anhui Medical University, Hefei 230032, China.
Abstract:
Rheumatoid arthritis (RA) represents a chronic autoimmune disease in which fibroblast-like synoviocytes (FLS) are pivotal contributors to disease pathogenesis. Reportedly, BMP9 inhibits the proliferation and migration of FLS in adjuvant-induced arthritis (AIA). Herein, we examined whether BMP9 suppresses the inflammatory response of RA FLS. The experimental results demonstrated a significant downregulation of BMP9 in RA synovial tissues, exhibiting an inverse correlation with TNF-α expression patterns. BMP9 silencing exacerbated TNF-α-mediated inflammatory responses in RA FLS, leading to substantial upregulation of IL-1β, IL-6, CXCL2, CXCL3, and CXCL5 expression levels. Conversely, BMP9 overexpression attenuated the inflammatory responses following stimulation with TNF-α and blocked the expression of IL-1β, IL-6, CXCL2, CXCL3, and CXCL5. Furthermore, BMP9 overexpression differentially regulated Smad signaling pathways by downregulating p-Smad2/3 while enhancing p-Smad1/5/9 activation. These findings demonstrate that BMP9 exerts anti-inflammatory effects in RA FLS by modulating Smad-dependent signaling pathways.
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