Objective: To investigate the impact of IGJ on the proliferation, inflammation, and motility of rheumatoid arthritis (RA) fibroblast-like synoviocytes and elucidate the underlying mechanism.
Methods: The expression of IGJ RA fibroblast-like synoviocytes was assessed using immunoblot and qPCR. Cell growth was evaluated using CCK-8 and FCM assays. The effects on inflammatory response were determined by ELISA and immunoblot assays. Cell motility was assessed using transwell and immunoblot assays. The mechanism was further confirmed using immunoblot assays.
Results: IGJ expression was found to be elevated in fibroid synovial cells of RA. IGJ ablation inhibited the growth of MH7A cells and suppressed the inflammatory response. Knockdown of IGJ also blocked cell motility. Mechanically, the knockdown of IGJ suppressed the NF-κB axis in MH7A cells.
Conclusion: IGJ suppresses RA in fibroblast-like synoviocytes via NF-κB pathway.
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http://dx.doi.org/10.1111/1756-185X.15282 | DOI Listing |
Int J Mol Sci
January 2025
Department of Physiology, Pomeranian Medical University, 70-111 Szczecin, Poland.
Rheumatoid arthritis (RA) is a chronic autoimmune disease that leads to joint damage and physical dysfunction. The pathogenesis of RA is highly complex, involving genetic, epigenetic, immune, and metabolic factors, among others. Over the years, research has highlighted the importance of non-coding RNAs (ncRNAs) in regulating gene expression.
View Article and Find Full Text PDFJ Pers Med
January 2025
Department of Applied Science, South East Technological University, R93 V960 Carlow, Ireland.
This study investigated the inflammatory responses of fibroblast-like synoviocytes (FLS) isolated from osteoarthritis (OA) patients, stimulated with lipopolysaccharide (LPS) and interleukin-6 (IL-6). Both experimental and synthetic data were utilised to investigate the variability in IL-6 and myeloperoxidase (MPO) production and its implications for OA pathogenesis. Synovial biopsies were obtained from OA patients undergoing joint replacement surgery.
View Article and Find Full Text PDFJ Orthop Surg Res
January 2025
Department of Rheumatology, Lanzhou University Second Hospital, Lanzhou University, No. 80, Cuiyingmen, Chengguan District, Lanzhou, Gansu Province, 730030, China.
Rheumatoid arthritis (RA) is a prevalent autoimmune disorder primarily targeting the diarthrodial joints. During the progression of RA, fibroblast-like synoviocytes (FLSs) exhibit tumor-like behavior, including increased proliferation, inflammation mediation, and aggressive phenotypes, leading to bone erosion. Additionally, T cells in RA acquire pro-inflammatory characteristics, exacerbating the inflammatory environment in affected joints and associated tissues.
View Article and Find Full Text PDFEpigenomes
January 2025
Department of Physiology, Pomeranian Medical University, 70-111 Szczecin, Poland.
Rheumatoid arthritis (RA) is a progressive autoimmune disease leading to structural and functional joint damage and, eventually, to physical disability. The pathogenesis of the disease is highly complex and involves interactions between fibroblast-like synoviocytes (FLSs) and immune cells, which stimulate the secretion of pro-inflammatory factors, leading to chronic inflammation. In recent years, studies have demonstrated the importance of epigenetics in RA.
View Article and Find Full Text PDFPhytomedicine
January 2025
First School of Clinical Medicine, Yunnan University of Chinese Medicine, Kunming 650500, China. Electronic address:
Background: Syringin (SRG) is well-known for its anti-inflammatory effects. However, its pharmacological mechanisms against rheumatoid arthritis (RA) are not fully understood.
Materials And Methods: We assessed the anti-RA effects of SRG using a collagen-induced arthritis (CIA) rat model.
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