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TGF ‐β3‐induced miR‐494 inhibits macrophage polarization via suppressing PGE 2 secretion in mesenchymal stem cells
Author(s) -
Zhao Guangfeng,
Miao Huishuang,
Li Xiujun,
Chen Shiwen,
Hu Yali,
Wang Zhiqun,
Hou Yayi
Publication year - 2016
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1002/1873-3468.12200
Subject(s) - macrophage polarization , mesenchymal stem cell , secretion , microbiology and biotechnology , chemistry , microrna , macrophage , m2 macrophage , immune system , downregulation and upregulation , andrology , immunology , biology , medicine , in vitro , biochemistry , gene
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 ( dMSC s) could regulate macrophage polarization. However, mi RNA in dMSC s of PE were maladjusted. Therefore, we speculated that mi RNA may affect dMSC ‐regulated macrophage polarization. In this study, we found that miR‐494‐overexpressed dMSC s inhibit M2 macrophage polarization and this inhibitory effect is mediated by miR‐494‐reduced PGE 2 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 dMSC s and attenuates the regulation of MSC switching the macrophage toward M2 type, contributing to an immune imbalance at maternal–fetal interface.