Department of Rheumatology, The Third Clinical College of Wenzhou Medical University, Wenzhou People's Hospital, Wenzhou, China.
Department of Pharmacy, The Third Clinical College of Wenzhou Medical University, Wenzhou People's Hospital, Wenzhou, China.
Arch Physiol Biochem. 2022 Dec;128(6):1426-1433. doi: 10.1080/13813455.2020.1773862. Epub 2020 Jun 17.
Several studies have suggested that fibroblast-like synoviocytes (FLSs) and miRNAs are implicated in the pathogenesis of rheumatoid arthritis (RA). This study was aimed to evaluate the function of miR-6089 in the regulation of RA-FLSs. The levels of miR-6089 were detected to be significantly lower in the synovial tissues and FLSs of RA than in the healthy synovial tissues and FLSs. The miR-6089 up-regulation in RA-FLSs significantly inhibited the proliferation and promoted cell apoptosis accompany with an increase protein expression of cleaved-Caspase-3, -8 and -9. Furthermore, CCR4 was determined to target miR-6089 directly, and its expression was significantly increased in the synovial tissues of RA than in the healthy synovial tissues. The overexpression of CCR4 reversed the effect of miR-6089 on proliferation and apoptosis in RA-FLSs effectively. In conclusion, our study suggests that the miR-6089 may be a potential target for prevention and treatment of RA.
几项研究表明，成纤维样滑膜细胞（FLSs）和 microRNA（miRNA）与类风湿关节炎（RA）的发病机制有关。本研究旨在评估 miR-6089 在调节 RA-FLSs 中的作用。结果显示，与健康滑膜组织和 FLSs 相比，RA 的滑膜组织和 FLSs 中 miR-6089 的水平明显降低。在 RA-FLSs 中上调 miR-6089 可显著抑制增殖，并促进细胞凋亡，同时伴有 cleaved-Caspase-3、-8 和 -9 蛋白表达增加。此外，CCR4 被确定可直接靶向 miR-6089，并且其在 RA 的滑膜组织中的表达明显高于健康的滑膜组织。CCR4 的过表达可有效逆转 miR-6089 对 RA-FLSs 增殖和凋亡的作用。综上所述，本研究表明 miR-6089 可能是预防和治疗 RA 的潜在靶点。
