miR-410-3p Suppresses Cytokine Release from Fibroblast-Like Synoviocytes by Regulating NF-κB Signaling in Rheumatoid Arthritis.
miR-410-3p Suppresses Cytokine Release from Fibroblast-Like Synoviocytes by Regulating NF-κB Signaling in Rheumatoid Arthritis.
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miR-410-3p通过调节类风湿关节炎中的NF-κB信号传导来抑制成纤维细胞样的滑膜细胞的细胞因子释放。
DOI：
10.1007/s10753-018-0896-2
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发表时间：
2019-03
期刊：
影响因子：
5.1
通讯作者：
Zhang N
中科院分区：
文献类型：
--
作者：
Wang Y;Xu N;Zhao S;Jiao T;Fu W;Yang L;Zhang N
miR-410- 3 p在某些恶性肿瘤中作为癌基因或肿瘤抑制基因发挥作用。然而，其在类风湿性关节炎（RA）中的作用尚不清楚。本研究旨在探讨miR-410- 3 p在RA发病机制中的作用。采用实时荧光定量RT-PCR法检测滑膜组织和成纤维细胞样滑膜细胞（FLS）中miR-410- 3 p的mRNA水平。采用ELISA检测肿瘤坏死因子（TNF）-α、白细胞介素（IL）-1β、IL-6和基质金属蛋白酶（MMP）-9的产生水平。采用蛋白质印迹法测定IκB-α、p-IκBα、p65和p-p65的蛋白水平。采用核因子（NF）-κB活化和核转位试验证实NF-κB活化。我们发现miR-410- 3 p在RA滑膜组织和FLS中的表达水平下调。miR-410- 3 p的过表达显著降低了人RA成纤维细胞样滑膜细胞（HFLS-RA）中TNF-α、IL-1β、IL-6和MMP-9的分泌;而miR-410- 3 p的抑制增加了这些细胞因子的表达水平。此外，miR-410- 3 p还能抑制NF-κB信号通路的激活。此外，NF-κB抑制剂恢复了由miR-410- 3 p抑制诱导的TNF-α、IL-1β、IL-6和MMP-9的升高。我们的研究结果表明miR-410- 3 p通过调节NF-κB信号通路在RA的发病机制中起炎症抑制作用。这些数据提示了miR-410- 3 p的新功能，并为RA中涉及的复杂机制提供了见解。
miR-410-3p acts as an oncogene or a tumor suppressor in some malignancies. However, its role in rheumatoid arthritis (RA) is unknown. The study was conducted to investigate the effect of miR-410-3p on the pathogenesis of RA. Real-time RT-PCR was used to determine the mRNA levels of miR-410-3p in synovial tissues and fibroblast-like synoviocytes (FLSs). An ELISA was performed to examine the production levels of tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, and matrix metalloproteinase (MMP)-9. Western blotting was conducted to determine the protein levels of IκB-α, p-IκBα, p65, and p-p65. Nuclear factor (NF)-κB activation and nuclear translocation assays were performed to confirm the activation of NF-κB. We found that the expression level of miR-410-3p was downregulated in synovial tissues and FLSs from RA. Overexpression of miR-410-3p significantly reduced the secretion of TNF-α, IL-1β, IL-6, and MMP-9 in human RA fibroblast-like synoviocytes (HFLS-RA); whereas miR-410-3p inhibition increased the expression levels of these cytokines. Furthermore, miR-410-3p suppresses the activation of NF-κB signaling pathway. Moreover, NF-κB inhibitor restored the elevation of TNF-α, IL-1β, IL-6, and MMP-9 induced by miR-410-3p inhibition. Our results demonstrate that miR-410-3p acts an inflammatory suppressor in the pathogenesis of RA by regulating the NF-κB signaling pathway. These data suggest a novel function of miR-410-3p and provide insight into the complex mechanisms involved in RA.
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影响因子：
4.9
作者：
Dasuri K;Antonovici M;Chen K;Wong K;Standing K;Ens W;El-Gabalawy H;Wilkins JA
通讯作者：
Wilkins JA
影响因子：
3.4
作者：
Liu, Chunyuan;Zhang, Aihong;Gao, Yang
通讯作者：
Gao, Yang
影响因子：
44.1
作者：
通讯作者：
--
影响因子：
8
作者：
Chien, W. W.;Domenech, C.;Ffrench, M.
通讯作者：
Ffrench, M.
人脐带间充质干细胞来源的细胞外囊泡通过转移 miR-410 促进肺腺癌生长。
影响因子：
9
作者：
Dong L;Pu Y;Zhang L;Qi Q;Xu L;Li W;Wei C;Wang X;Zhou S;Zhu J;Wang X;Liu F;Chen X;Su C
通讯作者：
Su C