MicroRNA-93 inhibits inflammatory cytokine production in LPS-stimulated murine macrophages by targeting IRAK4
MicroRNA-93 inhibits inflammatory cytokine production in LPS-stimulated murine macrophages by targeting IRAK4
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MicroRNA-93 通过靶向 IRAK4 抑制 LPS 刺激的小鼠巨噬细胞中炎症细胞因子的产生
DOI：
10.1016/j.febslet.2014.03.013
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发表时间：
2014-05-02
期刊：
影响因子：
3.5
通讯作者：
Xu, Xun
中科院分区：
文献类型：
--
作者：
Xu, Yan;Jin, Huiyi;Xu, Xun
内毒素诱导的葡萄膜炎（EIU）是一种用于研究人类内源性前葡萄膜炎的急性眼部炎症动物模型。眼部炎症发生发展的机制仍不清楚。MicroRNA（mi-RNA）已被提出作为新的炎症调节因子。目前尚不清楚microRNA介导的调节机制是否参与LPS诱导的EIU。在这项研究中，我们报告了miR-93在EIU大鼠和LPS刺激的巨噬细胞中的表达显著降低。我们还发现，miR-93通过靶向IRAK 4表达抑制NF-κ B活化和促炎细胞因子。我们进一步证明了miR-93通过直接结合IRAK 4的3 '-UTR来抑制IRAK 4表达。我们的研究结果表明，miR-93是EIU免疫反应的负调节因子。(C)2014年欧洲生物化学学会联合会。由Elsevier B出版。V.保留所有权利。
Endotoxin-induced uveitis (EIU) is an animal model of acute ocular inflammation for the study of human endogenous anterior uveitis. The mechanisms accounting for the development of ocular inflammation remain hazy. MicroRNAs (mi-RNAs) have been proposed as novel regulators of inflammation. It remains unclear whether a microRNA-mediated regulatory mechanism is involved in LPS-induced EIU. In this study, we report that miR-93 expression in the eyes of EIU rats and LPS-stimulated macrophages is significantly decreased. We also show that miR-93 inhibits NF-kappa B activation and pro-inflammatory cytokines by targeting IRAK4 expression. We further demonstrate that miR-93 inhibits IRAK4 expression by binding directly to the 3'-UTR of IRAK4. Our findings suggest that miR-93 is a negative regulator of the immune response in EIU. (C) 2014 Federation of European Biochemical Societies. Published by Elsevier B. V. All rights reserved.