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首页> 外文期刊>FEBS letters. >MiR-30a attenuates immunosuppressive functions of IL-1 beta-elicited mesenchymal stem cells via targeting TAB3
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MiR-30a attenuates immunosuppressive functions of IL-1 beta-elicited mesenchymal stem cells via targeting TAB3

机译:MiR-30a通过靶向TAB3减弱IL-1β诱导的间充质干细胞的免疫抑制功能

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摘要

Mesenchymal stem cells (MSCs) possess the ability to modulate the immune response, and their abnormalities are related to several diseases. We previously reported that miR-30a expression significantly increased in the maternal-fetal interface during preeclampsia (PE), but the effects of miR-30a on the immunoregulatory characteristics of MSCs are unclear. In this study, we determined that miR-30a over-expression inhibited the IL-1 beta-elicited activation of the nuclear factor kappa B (NF-kappa B) and JNK signaling pathways and the production of IL-6, cyclooxygenase 2 (COX2) and IL-8 by targeting transforming growth factor-beta-activated kinase 1 binding protein 3 (TAB3) in MSCs. Moreover, the over-expression of miR-30a also impaired MSCs' anti-inflammatory effects on macrophages. These data demonstrated that miR-30a in MSCs may participate in the immune dysregulation of the maternal-fetal interface during PE. (C) 2015 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
机译:间充质干细胞(MSCs)具有调节免疫反应的能力,其异常与几种疾病有关。我们先前报道先兆子痫(PE)期间母婴界面中miR-30a表达显着增加,但miR-30a对MSCs免疫调节特性的影响尚不清楚。在这项研究中,我们确定miR-30a过表达抑制了IL-1β诱导的核因子κB(NF-κB)和JNK信号通路的激活以及IL-6,环氧合酶2(COX2)的产生。 )和IL-8(通过靶向MSC中的转化生长因子-β-活化的激酶1结合蛋白3(TAB3))来实现。此外,miR-30a的过表达也损害了MSC对巨噬细胞的抗炎作用。这些数据表明,在PE期间,MSC中的miR-30a可能参与母胎界面的免疫失调。 (C)2015年欧洲生物化学学会联合会。由Elsevier B.V.发布。保留所有权利。

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