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• W2997863353 endingPage "106067" @default.
• W2997863353 startingPage "106067" @default.
• W2997863353 abstract "There is growing evidence of the ability of microRNAs (miRs) in rheumatoid arthritis (RA), thus our objective was to discuss the impact of miR-365 on the apoptosis and proliferation of synoviocytes in mice with RA by targeting IGF1 and mediating the PI3K/AKT/mTOR pathway. RA model mice was induced by type II collagen and freund’s adjuvant. The successfully modeled mice were injected with normal saline, miR-365 mimics, miR-365 inhibitors or their controls. TUNEL assay was adopted to detect apoptosis in synovial tissues, and expression of IL-1β and IL-6 in serum and synovial tissues was measured by ELISA and RT-qPCR. Mouse synoviocytes were isolated and cultured in vitro and identified by experiments. Cells were transfected with miR-365 mimics, IGF1 siRNA, or their controls to verify the role of miR-365 and IGF1 in cell vitality, proliferation and apoptosis of synoviocytes. Upregulation of miR-365 increased the number of TUNEL positive cells, depressed arthritis index, X-ray imaging score, and the expression of IL-1β and IL-6. High expression of miR-365 and low expression of IGF1 restrained the proliferation and facilitated apoptosis of synoviocytes. MiR-365 inhibited the expression of IGF1 and inhibited the activation of the PI3K/AKT/mTOR pathway. Our study presents that up-regulation of miR-365 drives on apoptosis and restrains proliferation of synoviocytes in RA through downregulation of IGF1 and the inhibition of the PI3K/AKT/mTOR pathway. Thus, miR-365 may be a potential candidate for treatment of RA." @default.
• W2997863353 created "2020-01-10" @default.
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• W2997863353 date "2020-02-01" @default.
• W2997863353 modified "2023-09-30" @default.
• W2997863353 title "Up-regulation of miR-365 promotes the apoptosis and restrains proliferation of synoviocytes through downregulation of IGF1 and the inactivation of the PI3K/AKT/mTOR pathway in mice with rheumatoid arthritis" @default.
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• W2997863353 doi "https://doi.org/10.1016/j.intimp.2019.106067" @default.
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