[Expression of miR-342-3p in rheumatoid arthritis patients and its effect on synovial fibroblast inflammation and migration]

[miR-342-3p在类风湿性关节炎患者中的表达及其对滑膜成纤维细胞炎症和迁移的影响]

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Abstract

OBJECTIVE: To investigate the expression level of miR-342-3p in peripheral blood mononuclear cells (PBMCs) of patients with rheumatoid arthritis (RA) and its effect on inflammatory response and migration of synovial fibroblasts in RA (RA-FLS). METHODS: PBMCs were collected from 30 healthy individuals and 50 RA patients for detecting the expression of miR-342-3p, and its correlation with the clinical indicators RF, ESR, anti-CCP, hs-CRP, C3, DAS-28, SAS, and SDS was analyzed. In RA-FLS cultures, the effect of transfection of miR-342-3p mimics and inhibitor on TNF-α-induced inflammatory response of the cells was evaluated by detecting the expressions of IL-1β, IL-6, IL-10, and TNF-α using ELISA. CCK8 assay and Transwell assay were used for detecting the changes in cell viability and migration ability of the synovial cells. RESULTS: In RA patients, the expression level of miR-342-3p was significantly lowered in the PBMCs (P < 0.05) with an area under the ROC curve of 97.53% and showed inverse correlations with RF (r=-0.321), ESR(r=-0.284), anti-CCP (r=-0.355), hs-CRP (r=-0.320), C3 (r=-0.294), DAS-28 (r=-0.395), SAS (r=-0.366), and SDS (r=-0.397) (all P < 0.05); a low expression of miR-342-3p was strongly associated with elevated levels of anti-CCP, DAS-28, SDS, and SAS (all with a rule support greater than 85%, confidence greater than 88%, and lift greater than 1). In cultured RA-FLS, TNF-α stimulation significantly increased the cell viability (P < 0.05), upregulated the expressions of IL-1β, IL-6, and TNF-α, and lowered the expression of IL-10 (P < 0.05). These changes were significantly suppressed by transfection of the cells with miR-342-3p mimics (P < 0.05) but enhanced by transfection with miR-342-3p inhibitor (P < 0.05). CONCLUSION: The expression of miR-342-3p is decreased in the PBMCs of RA patients. A lowered expression of miR-342-3p contributes to the pathogenesis of RA by promoting inflammatory responses and migration of RA-FLS.

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