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10.1186/s13000-015-0309-x

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C4472173!4472173!26088648
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suck abstract from ncbi


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pmid26088648      Diagn+Pathol 2015 ; 10 (ä): ä
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  • MicroRNA-26b inhibits cell proliferation and cytokine secretion in human RASF cells via the Wnt/GSK-3?/?-catenin pathway #MMPMID26088648
  • Sun J; Yan P; Chen Y; Chen Y; Yang J; Xu G; Mao H; Qiu Y
  • Diagn Pathol 2015[]; 10 (ä): ä PMID26088648show ga
  • Background: Rheumatoid arthritis (RA) is a chronic systemic auto- immune disease characterized by joint synovitis. Recent evidence suggests that rheumatoid arthritis synovial fibroblasts (RASFs) promote joint destruction. In this study, we investigated the role of microRNA-26b (miR-26b) in cell proliferation and inflammatory cytokine secretion using patient-derived Rheumatoid arthritis fibroblast-like synoviocyte (RAFLS) to understand pathways influencing rheumatoid arthritis. Methods: RAFLS were cultured in vitro and transfected with miR-26b mimics (experimental group) and negative sequence (control group). The protein levels of Wnt4, Wnt5?, GSK-3?, CyclinD1, Ser9-GSK-3? and ?-catenin were detected by western blot analysis. Tumor Necrosis Factor-? (TNF-?), IL- 1?, and IL-6 levels were quantified by Enzyme-linked Immunosorbent Assay (ELISA). RAFLS proliferation and apoptosis were measured by 3-[4, 5-dimethylthiazol-2-yl]-2, 5-diphenyl tetrazolium bromide (MTT) assay and flow cytometry, respectively. Results: GSK-3? and CyclinD1 expression levels were lower in miR-26b mimic group compared to Mock group and negative control (NC) group. Conversely, GSK-3? and CyclinD1 expression levels were markedly higher in the miR-26b inhibitor group compared to Mock and NC group (P?
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