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Abstract：
BACKGROUND: Rheumatoid arthritis (RA) is a chronic immune system disease with a high disability rate threatening the living quality of patients. Identifying potential biomarkers for RA is of necessity to improve the prevention and management of RA.
OBJECTIVE: This study focused on miR-146b-3p evaluating its clinical significance and revealing the underlying regulatory mechanisms.
METHODS: A total of 107 RA patients were enrolled, and both serum and synovial tissues were collected. Another 78 osteoarthritis patients (OA, providing synovial tissues), and 72 healthy individuals (providing serum samples) were enrolled as the control group. The expression of miR-146b-3p was analyzed by PCR and analyzed with ROC and Pearson correlation analyses evaluating its significance in diagnosis and development prediction of RA patients. In vitro, MH7A cells were treated with TNF-α. The regulation of cell proliferation, motility, and inflammation by miR-146b-3p was assessed by CCK8, Transwell, and ELISA assays.
RESULTS: Significant upregulation of miR-146b-3p was observed in serum and synovial tissues of RA patients, which distinguished RA patients and were positively correlated with the erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), anti-cyclic citrullinated peptide antibodies (anti-CCP), and rheumatoid factor (RF) of RA patients. TNF-α promoted the proliferation and motility of MH7A cells and induced significant inflammation in cells. Silencing miR-146b-3p alleviated the effect of TNF-α and negatively regulated the expression of HMGCR. The knockdown of HMGCR reversed the protective effect of miR-146b-3p silencing on TNF-α-stimulated MH7A cells.
CONCLUSIONS: Increased miR-146b-3p served as a biomarker for the diagnosis and severity of RA. Silencing miR-146b-3p could suppress TNF-α-induced excessive proliferation, motility, and inflammation via regulating HMGCR in MH7A cells.
OBJECTIVE: This study focused on miR-146b-3p evaluating its clinical significance and revealing the underlying regulatory mechanisms.
METHODS: A total of 107 RA patients were enrolled, and both serum and synovial tissues were collected. Another 78 osteoarthritis patients (OA, providing synovial tissues), and 72 healthy individuals (providing serum samples) were enrolled as the control group. The expression of miR-146b-3p was analyzed by PCR and analyzed with ROC and Pearson correlation analyses evaluating its significance in diagnosis and development prediction of RA patients. In vitro, MH7A cells were treated with TNF-α. The regulation of cell proliferation, motility, and inflammation by miR-146b-3p was assessed by CCK8, Transwell, and ELISA assays.
RESULTS: Significant upregulation of miR-146b-3p was observed in serum and synovial tissues of RA patients, which distinguished RA patients and were positively correlated with the erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), anti-cyclic citrullinated peptide antibodies (anti-CCP), and rheumatoid factor (RF) of RA patients. TNF-α promoted the proliferation and motility of MH7A cells and induced significant inflammation in cells. Silencing miR-146b-3p alleviated the effect of TNF-α and negatively regulated the expression of HMGCR. The knockdown of HMGCR reversed the protective effect of miR-146b-3p silencing on TNF-α-stimulated MH7A cells.
CONCLUSIONS: Increased miR-146b-3p served as a biomarker for the diagnosis and severity of RA. Silencing miR-146b-3p could suppress TNF-α-induced excessive proliferation, motility, and inflammation via regulating HMGCR in MH7A cells.
摘要：
背景：类风湿性关节炎（RA）是一种慢性免疫系统疾病，致残率高，威胁患者的生活质量。确定RA的潜在生物标志物对于改善RA的预防和管理是必要的。
目的：本研究集中于miR-146b-3p评估其临床意义并揭示其潜在的调控机制。
方法：共纳入107例RA患者，同时收集血清和滑膜组织。另78例骨关节炎患者（OA，提供滑膜组织)，和72名健康个体（提供血清样本）作为对照组。通过PCR分析miR-146b-3p的表达，并通过ROC和Pearson相关性分析评估其在RA患者诊断和发展预测中的意义。体外，用TNF-α处理MH7A细胞。细胞增殖的调节，运动性,和炎症miR-146b-3p通过CCK8，Transwell，和ELISA测定。
结果：在RA患者血清和滑膜组织中观察到miR-146b-3p显著上调，区分RA患者，与血沉（ESR）呈正相关，C反应蛋白(CRP),抗环瓜氨酸肽抗体（抗CCP），RA患者的类风湿因子（RF）。TNF-α促进MH7A细胞的增殖和运动，并在细胞中诱导明显的炎症。沉默miR-146b-3p减轻了TNF-α的作用，并负调控了HMGCR的表达。HMGCR的敲低逆转了miR-146b-3p沉默对TNF-α刺激的MH7A细胞的保护作用。
结论：增加的miR-146b-3p可作为RA诊断和严重程度的生物标志物。沉默miR-146b-3p可以抑制TNF-α诱导的过度增殖,运动性,而炎症则经由过程调控MH7A细胞中的HMGCR。
目的：本研究集中于miR-146b-3p评估其临床意义并揭示其潜在的调控机制。
方法：共纳入107例RA患者，同时收集血清和滑膜组织。另78例骨关节炎患者（OA，提供滑膜组织)，和72名健康个体（提供血清样本）作为对照组。通过PCR分析miR-146b-3p的表达，并通过ROC和Pearson相关性分析评估其在RA患者诊断和发展预测中的意义。体外，用TNF-α处理MH7A细胞。细胞增殖的调节，运动性,和炎症miR-146b-3p通过CCK8，Transwell，和ELISA测定。
结果：在RA患者血清和滑膜组织中观察到miR-146b-3p显著上调，区分RA患者，与血沉（ESR）呈正相关，C反应蛋白(CRP),抗环瓜氨酸肽抗体（抗CCP），RA患者的类风湿因子（RF）。TNF-α促进MH7A细胞的增殖和运动，并在细胞中诱导明显的炎症。沉默miR-146b-3p减轻了TNF-α的作用，并负调控了HMGCR的表达。HMGCR的敲低逆转了miR-146b-3p沉默对TNF-α刺激的MH7A细胞的保护作用。
结论：增加的miR-146b-3p可作为RA诊断和严重程度的生物标志物。沉默miR-146b-3p可以抑制TNF-α诱导的过度增殖,运动性,而炎症则经由过程调控MH7A细胞中的HMGCR。
