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10.1186/s13000-015-0309-x http://scihub22266oqcxt.onion/10.1186/s13000-015-0309-x C4472173!4472173 !26088648     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26088648 &cmd=llinks): Failed to open stream: HTTP request failed! 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MicroRNA-26b inhibits cell proliferation and cytokine secretion in human RASF cells via the Wnt/GSK-3?/?-catenin pathway |pdf=|usr=}}{{26088648 }} gab.com Text MicroRNA-26b inhibits cell proliferation and cytokine secretion in human RASF cells via the Wnt/GSK-3 / -catenin pathway JO: Diagn Pathol http://www.kidney.de/pget.php?&tw=1&pmid=26088648 #FOAvip 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?<?0.05). Transfection of miR-26b mimics significantly increased the, levels of Ser9-GSK-3? and ?-catenin in comparison to Mock and NC groups, while transfection of miR-26b inhibitors showed the opposite effect. In miR-26b mimic group, TNF-?, IL- 1? and IL-6 levels were lower than the Mock and NC groups, while in miR-26b inhibitor group, these cytokine levels were higher than the Mock and NC groups (P?<?0.05). Transfection of miR-26b mimics significantly reduced the cell proliferation of RAFLS, compared to the Mock and NC groups, and miR-26b inhibitors increased the proliferative capacity of RAFLS compared to Mock and NC groups (P?<?0.05). The miR-26b mimic group exhibited higher RAFLS apoptosis rate compared to Mock and NC group and miR-26b inhibitor group showed significantly lower RAFLS apoptosis rate compared to Mock and NC groups (P?<?0.05). CONCLUSIONS: MiR-26b regulates ?-catenin and CyclinD1 levels by inhibiting GSK-3? expression, which in-turn alters the Wnt/GSK-3?/?-catenin pathway to lower RAFLS proliferation and elevate cell apoptosis and the secretion of TNF-?,IL-1? and IL-6 cytokines. Therefore, our results show that miR-26B plays a central role in inhibiting the inflammation associated with rheumatoid arthritis. VIRTUAL SLIDES: The virtual slide(s) for this article can be found here: http://www.diagnosticpathology.diagnomx.eu/vs/9063056861547150. Twit Text FOAVip MicroRNA-26b inhibits cell proliferation and cytokine secretion in human RASF cells via the Wnt/GSK-3 / -catenin pathway ????Diagn Pathol http://www.kidney.de/pget.php?&tw=1&pmid=26088648 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26088648 #FOAvip English Wikipedia <ref>{{Cite pmid|26088648 }}</ref> 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[Jun]; 10 (ä): 72 PMID26088648 show 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? |*Cell Proliferation [MESH] |*Wnt Signaling Pathway [MESH] |Apoptosis [MESH] |Arthritis, Rheumatoid/*enzymology/genetics/pathology [MESH] |Blotting, Western [MESH] |Cells, Cultured [MESH] |Cyclin D1/metabolism [MESH] |Cytokines/*metabolism [MESH] |Enzyme-Linked Immunosorbent Assay [MESH] |Fibroblasts/*enzymology/metabolism/pathology [MESH] |Genes, Reporter [MESH] |Glycogen Synthase Kinase 3 beta [MESH] |Glycogen Synthase Kinase 3/*metabolism [MESH] |Humans [MESH] |MicroRNAs/genetics/*metabolism [MESH] |Real-Time Polymerase Chain Reaction [MESH] |Reverse Transcriptase Polymerase Chain Reaction [MESH] |Synovial Membrane/*enzymology/metabolism/pathology [MESH] |Transfection [MESH]MicroRNA-26b inhibits cell proliferation and cytokine secretion in hum(epmc).pdf DeepDyve Pubget Overpricing