Analysis of immune regulation by dioxin receptor via induction of microRNA

二恶英受体通过 microRNA 诱导的免疫调节分析

• 批准号: 24790471
• 负责人: グェン ナム
• 金额: $ 2.83万
• 依托单位: Osaka University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Young Scientists (B)
• 财政年份: 2012
• 资助国家: 日本
• 起止时间: 2012 至 2013
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-24790471/
• 关键词: ダイオキシン受容体; miR-132/miR-212クラスター; マクロファージ; アリル炭化水素受容体; 免疫制御

We demonstrated that miR-132/miR-212 cluster double knock-out mice are hypersensitive to LPS than WT mice. We showed miR-132/miR-212 cluster is up-regulated in peritoneal macrophages but not in M1 or M2 macrophages in the stimulation of LPS. LPS-induced upregulation of miR-132/miR-212 cluster is suppressed in Ahr knock-out peritoneal macrophages compared to WT cells. We also demonstrated that IL-6 could be a direct target of miR-132/miR-212 cluster. Therefore, Ahr-dependent miR-132/miR-212 negatively regulates LPS-induced IL-6 in peritoneal macrophages.

我们证明了miR-132/miR-212簇双敲除小鼠比WT小鼠对LPS过敏。我们发现在LPS刺激下，miR-132/miR-212簇在腹腔巨噬细胞中上调，但在M1或M2巨噬细胞中不上调。与WT细胞相比，LPS诱导的miR-132/miR-212簇的上调在Ahr敲除的腹膜巨噬细胞中受到抑制。IL-6可能是miR-132/miR-212簇的直接靶点。因此，Ahr依赖性miR-132/miR-212负调节腹腔巨噬细胞中LPS诱导的IL-6。

项目成果

MiR-132/212 induction is involved in M1 differentiation through an Ahr-dependent mechanism

MiR-132/212 诱导通过 Ahr 依赖性机制参与 M1 分化

• 发表时间: 2012
• 作者: Gray;E.E.;Friend;S.;Suzuki;K.;Phan;T.G. and Cyster;J.G.;Kazuhiro Suzuki;Kazuhiro Suzuki;Nam T. Nguyen et al.
• 通讯作者: Nam T. Nguyen et al.