Identification of MyD88 as a novel target of miR-155, involved in negative regulation of Helicobacter pylori-induced inflammation

Identification of MyD88 as a novel target of miR-155, involved in negative regulation of Helicobacter pylori-induced inflammation
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鉴定 MyD88 作为 miR-155 的新靶标,参与幽门螺杆菌诱导的炎症的负调节

DOI:
10.1016/j.febslet.2010.02.063
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发表时间:
2010-04-16
期刊:
影响因子:
3.5
通讯作者:
Mao, Xu-Hu
Mao, Xu-Hu
中科院分区:
生物学3区
文献类型:
--
作者:
Tang, Bin;Xiao, Bin;Mao, Xu-Hu

文献摘要

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MicroRNA-155(miR-155)被认为是免疫系统的中枢调节因子。我们以前曾报道过miR-155负调控幽门螺杆菌(H. pylori)诱导的炎症,但miR-155调控炎症的分子机制尚不完全清楚。在这里,我们确定髓样分化蛋白88(MyD 88)作为miR-155的靶基因,并发现miR-155在蛋白质而不是mRNA信息水平上降低MyD 88的表达,这表明miR-155介导的抑制是转录后事件。此外,miR-155的过表达导致H.幽门感染因此,我们已经证明miR-155可以通过靶向炎症途径中的关键衔接分子MyD 88来负调控炎症。(C)2010年欧洲生物化学学会联合会。由Elsevier B出版。V.保留所有权利。
MicroRNA-155 (miR-155) has been implicated as a central regulator of the immune system. We have previously reported that miR-155 negatively regulates Helicobacter pylori (H. pylori)-induced inflammation, but the molecular mechanism of miR-155 regulating the inflammation is not fully clear. Here, we identified myeloid differentiation protein 88 (MyD88) as a target gene of miR-155, and found that miR-155 decreased MyD88 expression at the protein but not the mRNA message level, suggesting that the miR-155-mediated inhibition is a post-transcriptional event. Furthermore, the overexpression of miR-155 led to significantly reduced IL-8 production induced by H. pylori infection. Thus, we have demonstrated that miR-155 can negatively regulate inflammation by targeting a key adaptor molecule MyD88 in inflammatory pathways. (C) 2010 Federation of European Biochemical Societies. Published by Elsevier B. V. All rights reserved.