TGF-β3-induced miR-494 inhibits macrophage polarization via suppressing PGE2 secretion in mesenchymal stem cells

被引：47
|
作者：
Zhao, Guangfeng [1 ]
Miao, Huishuang [2 ]
Li, Xiujun [1 ]
Chen, Shiwen [1 ]
Hu, Yali [1 ,3 ]
Wang, Zhiqun [1 ]
Hou, Yayi [2 ,3 ]
机构：
[1] Nanjing Univ, Nanjing Drum Tower Hosp, Dept Obstet & Gynecol, Sch Med, Nanjing 210008, Jiangsu, Peoples R China
[2] Nanjing Univ, State Key Lab Pharmaceut Biotechnol, Div Immunol, Sch Med, Nanjing 210093, Jiangsu, Peoples R China
[3] Jiangsu Key Lab Mol Med, Nanjing, Jiangsu, Peoples R China
来源：
FEBS LETTERS | 2016年 / 590卷 / 11期
基金：
中国国家自然科学基金;
关键词：
macrophage polarization; mesenchymal stem cell; miR-494; preeclampsia; TGF-beta; 3; INDUCIBLE FACTOR-I; TROPHOBLAST DIFFERENTIATION; DECIDUAL MACROPHAGES; M2; MACROPHAGES; PREECLAMPSIA; MICRORNA-494; GROWTH; PROLIFERATION; EXPRESSION; PHENOTYPE;
D O I：
10.1002/1873-3468.12200
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
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-beta 3. In summary, our findings suggest that the high expression of TGF-beta 3 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.
引用
收藏
页码：1602 / 1613
页数：12
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