丙酸钠通过促进miR-140-5p抑制生存素介导的成纤维细胞样滑膜细胞增殖改善类风湿性关节炎

IF 3.3 4区 医学 Q3 IMMUNOLOGY
Sha Ma, Jing Wang, Fang He, Dachen Zuo, Fayou Li, H. Fan, Z. Yin, H. Liang, Qin Li
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引用次数: 6

摘要

摘要背景成纤维细胞样滑膜细胞增殖增加和死亡受损在类风湿性关节炎(RA)的发展中起着重要作用。Survivin在RA的前驱期和预后中起着重要作用,并已被引入作为RA患者关节损伤的生物标志物。本研究的目的是探讨丙酸盐是否通过miR-140-5p/survivin途径减轻RA。方法收集RA患者滑膜组织,检测miR-140-5p和survivin的表达水平;用10 mM丙酸钠(SP),然后检测miR-140-5p和生存素的表达、细胞活力和凋亡;构建胶原诱导性关节炎(CIA)大鼠模型,用SP治疗,检测组织炎症水平及miR-140-5p和Survivin的表达水平。结果RA患者滑膜组织和RA FLSs细胞中miR-140-5p的表达降低,而生存素的表达显著增加。SP可促进RA FLSs细胞中miR-140-5p的表达和凋亡,并抑制RAFLSS细胞生存素的表达和细胞活力。此外,miR-140-5p通过靶向生存素发挥保护作用。重要的是,在CIA大鼠模型中,SP降低了关节炎症反应,miR-140-5p抑制剂削弱了SP的保护作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Sodium propionate improves rheumatoid arthritis by inhibiting survivin mediated proliferation of fibroblast like synoviocytes by promoting miR-140-5p
Abstract Background Increased proliferation and impaired death of fibroblast-like synovial cells play an important role in the development of rheumatoid arthritis (RA). Survivin plays an important role in the prodromal stage and prognosis of RA and has been introduced as a biomarker of joint injury in RA patients. The purpose of this study was to explore whether propionate alleviates RA through miR-140-5p/survivin pathway. Methods The synovial tissues of RA patients were collected to detect the expression levels of miR-140-5p and survivin; normal human fibroblast-like synovial cells (HLSs) and RA fibroblast-like synovial cells (RA-FLSs) were cultured and treated with 10 mM of sodium propionate (SP), then the expressions of miR-140-5p and survivin, cell viability and apoptosis were detected; collagen induced arthritis (CIA) rat model was constructed and treated with SP, then the tissue inflammation level and the expression levels of miR-140-5p and Survivin were detected. Results The expression of miR-140-5p decreased in synovial tissues of RA patients and RA-FLSs cells, while the expression of survivin increased significantly in RA patients. SP promoted miR-140-5p expression and apoptosis in RA-FLSs cells and inhibited survivin expression and cell viability of RA-FLSs cells. In addition, miR-140-5p plays a protective role by targeting survivin. Importantly, in the CIA rat model, SP reduced joint inflammatory response, and the miR-140-5p inhibitor weakened the protective effect of SP. Conclusion SP can alleviate RA by promoting the expression of miR-140-5p and inhibiting the excessive proliferation and death impairment of RA-FLSs cells induced by survivin.
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来源期刊
Autoimmunity
Autoimmunity 医学-免疫学
CiteScore
5.70
自引率
8.60%
发文量
59
审稿时长
6-12 weeks
期刊介绍: Autoimmunity is an international, peer reviewed journal that publishes articles on cell and molecular immunology, immunogenetics, molecular biology and autoimmunity. Current understanding of immunity and autoimmunity is being furthered by the progress in new molecular sciences that has recently been little short of spectacular. In addition to the basic elements and mechanisms of the immune system, Autoimmunity is interested in the cellular and molecular processes associated with systemic lupus erythematosus, rheumatoid arthritis, Sjogren syndrome, type I diabetes, multiple sclerosis and other systemic and organ-specific autoimmune disorders. The journal reflects the immunology areas where scientific progress is most rapid. It is a valuable tool to basic and translational researchers in cell biology, genetics and molecular biology of immunity and autoimmunity.
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