MiRNA-126 expression inhibits IL-23R mediated TNF-α or IFN-γ production in fibroblast-like synoviocytes in a mice model of collagen-induced rheumatoid arthritis.

MiRNA-126 expression inhibits IL-23R mediated TNF-α or IFN-γ production in fibroblast-like synoviocytes in a mice model of collagen-induced rheumatoid arthritis.
复制标题

DOI:
10.1007/s10495-018-1474-7
复制
发表时间:
2018-12
期刊:
Apoptosis : an international journal on programmed cell death
影响因子:
--
通讯作者:
Zhao D
Zhao D
中科院分区:
其他
文献类型:
--
作者:
Gao J;Kong R;Zhou X;Ji L;Zhang J;Zhao D

文献摘要

参考文献

被引文献

相似文献

miR-126和IL-23 R均影响类风湿关节炎(RA)的进程。本研究旨在探讨miR-126与IL-23 R的相关性以及miR-126对RA发病机制的可能调控作用。收集RA患者血清、滑膜组织和滑液,检测miR-126、IL-23 R、TNF-α和IFN-γ的表达。采用胶原诱导的关节炎小鼠模型建立成纤维样滑膜细胞(FLS)。使用编码pro-miR-126和anti-miR-126的慢病毒质粒或miR-126激动剂和相应的阴性对照手动干预miR-126的表达。与对照组相比,RA患者miR-126的表达受到抑制(P < 0.05)。RA患者TNF-α、IFN-γ的产生及IL-23 R的表达均显著高于对照组(P < 0.05)。在经pro-miR-126处理的FLS细胞中,给予pro-miR-126质粒上调miR-126,但抑制IL-23 R、TNF-α和IFN-γ的表达或产生。此外,miR-126激动剂逆转了抗miR-126质粒对FLS的影响。这些结果表明miR-126负调控IL-23 R、TNF-α和IFN-γ的表达。这些结果表明miR-126对RA进程的关键影响。此外,pro-miR-126有可能成为治疗RA的潜在药物。
Both miR-126 and IL-23R affect rheumatoid arthritis (RA) procession. This study aimed to investigate the association of miR-126 and IL-23R and the possible modulation of miR-126 to RA pathogenesis. Serum, synovial tissue and synovial fluid were collected from patients with RA, and expression of miR-126, IL-23R, TNF-α and IFN-γ were detected. Fibroblast-like synoviocytes (FLS) was established using a collagen-induced arthritis mice model. The expression of miR-126 was manual intervened using pro-miR-126 and anti-miR-126 encoding lentivirus plasmids, or miR-126 agonists and corresponding negative controls. MiR-126 expression was inhibited in RA patients when compared with controls (P < 0.05). TNF-α and IFN-γ production and IL-23R expression were significantly upregulated in RA patients when compared to controls (P < 0.05). In pro-miR-126 treated FLS cells, the administration of pro-miR-126 plasmids upregulated miR-126, but inhibited IL-23R, TNF-α and IFN-γ expression or production. Moreover, the miR-126 agonist reversed the effects of the anti-miR-126 plasmid on FLS. These results revealed that miR-126 negative regulated the expression of IL-23R, TNF-α and IFN-γ. These results suggest the key impact of miR-126 on RA procession. Moreover, pro-miR-126 might be explored to be a potential therapy for RA.
DOI: 10.1038/ni.3579
发表时间: 2017-01
期刊: Nature immunology
影响因子: 30.5
作者:
通讯作者: --
波兰风湿关节炎患者的IL-17A,IL-17F和IL-23R基因多态性。
DOI: 10.1007/s00005-014-0319-5
发表时间: 2015-06
影响因子: 3.2
作者:
Bogunia-Kubik, Katarzyna;Swierkot, Jerzy;Malak, Anna;Wysoczanska, Barbara;Nowak, Beata;Bialowas, Katarzyna;Gebura, Katarzyna;Korman, Lucyna;Wiland, Piotr
通讯作者: Wiland, Piotr
DOI: 10.4049/jimmunol.1203172
发表时间: 2013-05-01
期刊: Journal of immunology (Baltimore, Md. : 1950)
影响因子: --
作者:
Duhen R;Glatigny S;Arbelaez CA;Blair TC;Oukka M;Bettelli E
通讯作者: Bettelli E
DOI: 10.1084/jem.20030896
发表时间: 2003-12-15
期刊: The Journal of experimental medicine
影响因子: --
作者:
Murphy CA;Langrish CL;Chen Y;Blumenschein W;McClanahan T;Kastelein RA;Sedgwick JD;Cua DJ
通讯作者: Cua DJ
MicroRNA-126通过靶向PIK3R2并调节PI3K-AKT信号通路影响类风湿性关节炎滑膜成纤维细胞增殖和凋亡
DOI: 10.18632/oncotarget.12487
发表时间: 2016-11-08
期刊: Oncotarget
影响因子: --
作者:
Qu Y;Wu J;Deng JX;Zhang YP;Liang WY;Jiang ZL;Yu QH;Li J
通讯作者: Li J