MiR-30a attenuates immunosuppressive functions of IL-1β-elicited mesenchymal stem cells via targeting TAB3
MiR-30a attenuates immunosuppressive functions of IL-1β-elicited mesenchymal stem cells via targeting TAB3
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MiR-30a 通过靶向 TAB3 减弱 IL-1 β 诱导的间充质干细胞的免疫抑制功能
DOI：
10.1016/j.febslet.2015.11.001
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发表时间：
2015-12-21
期刊：
影响因子：
3.5
通讯作者：
Hou, Yayi
中科院分区：
文献类型：
--
作者：
Hu, Erling;Ding, Liang;Hou, Yayi
间充质干细胞（MSC）具有调节免疫反应的能力，其异常与多种疾病有关。我们之前报道，先兆子痫（PE）期间母胎界面中miR-30a的表达显着增加，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过表达通过靶向MSC中的转化生长因子-β激活激酶1结合蛋白3（TAB3）抑制IL-1β引起的核因子κB（NF-κB）和JNK信号通路的激活以及IL-6、环氧合酶2（COX2）和IL-8的产生。此外，miR-30a的过度表达也会损害MSCs对巨噬细胞的抗炎作用。这些数据表明，MSC 中的 miR-30a 可能参与 PE 期间母胎界面的免疫失调。 (C) 2015 年欧洲生化学会联合会。由 Elsevier B.V. 出版。保留所有权利。
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.