Department of Orthopaedics, The Affiliated Hospital of Southwest Medical University, Luzhou City, Sichuan Province 646000, P.R. China.
College of Pharmacy, Southwest Medical University, Luzhou City, Sichuan Province 646000, P.R. China
Biosci Rep. 2019 May 2;39(5). doi: 10.1042/BSR20182374. Print 2019 May 31.
IL-6 produced by human fibroblast-like synoviocytes (HFLS) promotes rheumatoid arthritis (RA), while lncRNA DILC regulates liver cancer stem cells by inhibiting IL-6. Therefore, lncRNA DILC may participate in RA. In the present study, we found that plasma lncRNA DILC was down-regulated, while IL-6 was up-regulated in RA patients than in healthy controls. Plasma levels of lncRNA DILC and IL-6 were significantly and inversely correlated only in RA patients. Overexpression of lncRNA DILC resulted in promoted apoptosis of HFLS isolated from RA patients, while lncRNA DILC siRNA silencing played an opposite role. In addition, overexpression of lncRNA DILC also resulted in inhibited IL-6 expression in HFLS isolated from RA patients. Therefore, lncRNA DILC may participate in RA by inducing apoptosis of HFLS and down-regulating IL-6.
人成纤维样滑膜细胞（HFLS）产生的白细胞介素 6（IL-6）促进类风湿关节炎（RA），而长链非编码 RNA DILC 通过抑制 IL-6 调节肝癌干细胞。因此，lncRNA DILC 可能参与 RA 的发生。本研究发现，与健康对照者相比，RA 患者的血浆 lncRNA DILC 下调，而 IL-6 上调。lncRNA DILC 和 IL-6 的血浆水平仅在 RA 患者中呈显著负相关。过表达 lncRNA DILC 导致 RA 患者分离的 HFLS 凋亡增加，而 lncRNA DILC siRNA 沉默则起到相反的作用。此外，过表达 lncRNA DILC 还导致 RA 患者分离的 HFLS 中 IL-6 表达下调。因此，lncRNA DILC 可能通过诱导 HFLS 凋亡和下调 IL-6 参与 RA 的发生。
