| Literature DB >> 27149081 |
Guangfeng Zhao1, Huishuang Miao2, Xiujun Li1, Shiwen Chen1, Yali Hu1,3, Zhiqun Wang1, Yayi Hou2,3.
Abstract
Abnormal macrophage polarization at the maternal-fetal interface may contribute to the development of Preeclampsia (PE). The reason why macrophage polarization changed in PE is still unclear. Decidual mesenchymal stem cells (dMSCs) could regulate macrophage polarization. However, miRNA in dMSCs of PE were maladjusted. Therefore, we speculated that miRNA may affect dMSC-regulated macrophage polarization. In this study, we found that miR-494-overexpressed dMSCs inhibit M2 macrophage polarization and this inhibitory effect is mediated by miR-494-reduced PGE2 secretion. Furthermore, we proved that miR-494 is induced by TGF-β3. In summary, our findings suggest that the high expression of TGF-β3 in PE decidua stimulates miR-494 in dMSCs and attenuates the regulation of MSC switching the macrophage toward M2 type, contributing to an immune imbalance at maternal-fetal interface.Entities:
Keywords: TGF-β3; macrophage polarization; mesenchymal stem cell; miR-494; preeclampsia
Mesh:
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Year: 2016 PMID: 27149081 DOI: 10.1002/1873-3468.12200
Source DB: PubMed Journal: FEBS Lett ISSN: 0014-5793 Impact factor: 4.124