Downregulation of miR-92a in Decidual Stromal Cells Suppresses Migration Ability of Trophoblasts by Promoting Macrophage Polarization.

IF 2.6 4区 生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY DNA and cell biology Pub Date : 2023-08-01 DOI:10.1089/dna.2022.0510
Huansheng Zhou, Hui Wang, Xiaohan Liu, Bei Liu, Yanci Che, Rendong Han
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引用次数: 1

Abstract

Preeclampsia (PE) is a severe pregnancy complication that accounts for about 14% of maternal deaths. Its clinical manifestations commonly include hypertension and proteinuria. However, it is largely limited in understanding its pathogenetic mechanism. In this study, we used bioinformatics to compare differential gene expressions in decidual stromal cells from PE patients and healthy donors. The result indicated that higher levels of CCL5 and CXCL2 were expressed in decidual stromal cells of PE patients compared with healthy pregnancy. The bioinformatics analysis confirmed that decidual stromal cells derived from PE patients expressed significantly lower miR-92a compared with those derived from healthy donors. Transfection of miR-92a inhibitors upregulated IL-6, CXCL2, CXCL3, CCL5, and CXCL8 expressions in decidual stromal cells. Luciferase activity assay confirmed that miR-92a directly targeted the mRNA of IRF3 whose overexpression could promote the secretion of cytokines. The flow cytometric analysis demonstrated that M1 macrophage infiltration was higher in the placentas of PE patients than in those of healthy donors. We also observed that after transfection of miR-92a inhibitor, condition medium (CM) derived from decidual stromal cells significantly promoted M1 polarization of macrophages. In addition, the transwell migration assay and flow cytometric analysis together showed that decidual stromal cell-derived CM induced macrophages to suppress the trophoblast migration and proliferation. Taken together, our result indicates that downregulation of miR-92a in decidual stromal cells promotes the macrophage polarization and suppresses the trophoblast migration and proliferation.

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蜕膜间质细胞中miR-92a下调通过促进巨噬细胞极化抑制滋养细胞迁移能力
先兆子痫(PE)是一种严重的妊娠并发症,约占孕产妇死亡的14%。其临床表现通常包括高血压和蛋白尿。然而,对其发病机制的认识在很大程度上是有限的。在这项研究中,我们使用生物信息学来比较PE患者和健康供者间质细胞的差异基因表达。结果表明,与健康妊娠相比,PE患者蜕膜间质细胞中CCL5和CXCL2表达水平较高。生物信息学分析证实,来自PE患者的蜕膜间质细胞与来自健康供者的蜕膜间质细胞相比,miR-92a的表达明显降低。转染miR-92a抑制剂可上调间质细胞中IL-6、CXCL2、CXCL3、CCL5和CXCL8的表达。荧光素酶活性测定证实miR-92a直接靶向IRF3 mRNA, IRF3过表达可促进细胞因子的分泌。流式细胞术分析显示,PE患者胎盘中M1巨噬细胞浸润高于健康供者。我们还观察到转染miR-92a抑制剂后,来自蜕质细胞的条件培养基(CM)显著促进巨噬细胞的M1极化。此外,跨井迁移实验和流式细胞术分析表明,蜕膜细胞源性CM诱导巨噬细胞抑制滋养细胞的迁移和增殖。综上所述,我们的研究结果表明,在蜕质细胞中下调miR-92a可促进巨噬细胞极化,抑制滋养细胞迁移和增殖。
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来源期刊
DNA and cell biology
DNA and cell biology 生物-生化与分子生物学
CiteScore
6.60
自引率
0.00%
发文量
93
审稿时长
1.5 months
期刊介绍: DNA and Cell Biology delivers authoritative, peer-reviewed research on all aspects of molecular and cellular biology, with a unique focus on combining mechanistic and clinical studies to drive the field forward. DNA and Cell Biology coverage includes: Gene Structure, Function, and Regulation Gene regulation Molecular mechanisms of cell activation Mechanisms of transcriptional, translational, or epigenetic control of gene expression Molecular Medicine Molecular pathogenesis Genetic approaches to cancer and autoimmune diseases Translational studies in cell and molecular biology Cellular Organelles Autophagy Apoptosis P bodies Peroxisosomes Protein Biosynthesis and Degradation Regulation of protein synthesis Post-translational modifications Control of degradation Cell-Autonomous Inflammation and Host Cell Response to Infection Responses to cytokines and other physiological mediators Evasive pathways of pathogens.
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