Our previous studies have identified miR-483-3p to be highly expressed in synoviocytes from patients with rheumatoid arhtirits (RA); however, its effects on inflammation of RA fibroblast-like synoviocytes (FLSs) have remained unclear. The expression of miR-483-3p and cytokines in RA FLSs was detected using quantitative real-time polymerase chain reaction. Enzyme-linked immunosorbent was conducted to determine interleukin (IL)-33 production from RA FLSs. Western blotting was employed to quantify the levels of p-ERK and total ERK. Overexpressed miR-483-3p significantly increased the mRNA and protein expression of IL-33, but not of IL-27 or IL-34, in RA FLSs, whereas miR-483-3p suppression showed the opposite effects. Furthermore, miR-483-3p upregulation activated the ERK signaling pathway. The ERK signaling inhibitor PD98059 partly reversed the elevation of IL-33 levels mediated by miR-483-3p overexpression. Our results reveal that miR-483-3p promotes IL-33 expression by regulating the ERK signaling pathway in RA FLSs. Thus, miR-483-3p may be a potential effective target for RA treatment.

我们之前的研究已经确定 miR-483-3p 在类风湿性关节炎 (RA) 患者的滑膜细胞中高表达；然而，其对 RA 成纤维细胞样滑膜细胞 (FLS) 炎症的影响仍不清楚。使用定量实时聚合酶链反应检测 RA FLS 中 miR-483-3p 和细胞因子的表达。进行酶联免疫吸附以确定 RA FLS 产生的白细胞介素 (IL)-33。Western印迹用于量化p-ERK和总ERK的水平。过表达的 miR-483-3p 显着增加了 RA FLS 中 IL-33 的 mRNA 和蛋白质表达，但不增加 IL-27 或 IL-34 的表达，而 miR-483-3p 抑制显示出相反的效果。此外，miR-483-3p 上调激活了 ERK 信号通路。ERK 信号抑制剂 PD98059 部分逆转了由 miR-483-3p 过表达介导的 IL-33 水平升高。我们的研究结果表明，miR-483-3p 通过调节 RA FLS 中的 ERK 信号通路促进 IL-33 表达。因此，miR-483-3p 可能是 RA 治疗的潜在有效靶点。