miR-483-3p promotes cell proliferation and suppresses apoptosis in rheumatoid arthritis fibroblast-like synoviocytes by targeting IGF-1 - 27/10/20
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Highlights |
• | Effect of miR-483−3p on RA FLSs proliferation, apoptosis, & cell cycle was studied. |
• | miR-483−3p levels were increased in synovium and FLSs of patients with RA. |
• | Up-regulated miR-483−3p promoted proliferation and suppressed apoptosis. |
• | Insulin-like growth factor 1 was verified as a direct target gene of miR-483−3p. |
• | Our findings might provide a potential therapeutic target for RA. |
Abstract |
Accumulating evidence suggests that miR-483−3p is implicated in maintaining biological properties in human cancers. However, its biological roles in rheumatoid arthritis (RA) remain unknown. miR-483−3p levels in synovial tissue samples and fibroblast-like synoviocytes (FLSs) were determined using quantitative real-time PCR. The CCK-8 assay and EdU staining were performed to assess cell proliferation in RA FLSs after transfection with miR-483−3p mimics or inhibitor. Flow cytometry with Annexin V-FITC staining or PI staining was performed to assess apoptosis or cell cycle progression in RA FLSs, respectively. miR-483−3p was upregulated in RA, which markedly promoted cell proliferation, induced the G0/G1-to-S phase transition, and suppressed apoptosis in RA FLSs, whereas miR-483−3p silencing yielded opposite results. Moreover, insulin growth factor 1 (IGF-1) was detected as a direct miR-483−3p target. IGF-1 silencing partially restored cell proliferation, the G0/G1-to-S phase transition, and apoptosis suppression in RA FLSs via miR-483−3p inhibition. Our results showed that miR-483−3p promotes RA FLSs proliferation by targeting IGF-1, suggesting a potential strategy for diagnostic and treatment strategy for RA.
Le texte complet de cet article est disponible en PDF.Abbreviations : RA, FLSs, miR, IGF-1, HFLS-RA, HFLS
Keywords : Rheumatoid arthritis, Synoviocytes, microRNA, Proliferation, Apoptosis
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