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miR-6869-5p 通过调控 PTPRO 在妊娠期糖尿病中诱导 M2 极化。

MiR-6869-5p Induces M2 Polarization by Regulating PTPRO in Gestational Diabetes Mellitus.

机构信息

Department of Gynecology and Obstetrics, the Affiliated Hospital of Maternal and Child Health, Weifang Medical University, Weifang 261000, China.

Department of Pharmacy, the First Affiliated Hospital of Weifang Medical University, Weifang 261000, China.

出版信息

Mediators Inflamm. 2021 Apr 30;2021:6696636. doi: 10.1155/2021/6696636. eCollection 2021.

Abstract

The role of microRNA (miRNA) in gestational diabetes mellitus has been widely investigated during the last decade. However, the altering effect of miR-6869-5p on immunity and placental microenvironment in gestational diabetes mellitus is largely unknown. In our study, the expression of miR-6869-5p was documented to be significantly decreased in placenta-derived mononuclear macrophages, which was also negatively related to PTPRO. Besides, PTPRO was negatively regulated by miR-6869-5p in placenta-derived mononuclear macrophages. In vitro, miR-6869-5p inhibited macrophage proliferation demonstrated by EdU and CCK-8 experiments. The inflammatory response in macrophages was also significantly inhibited by miR-6869-5p, which could regulate PTPRO as a target documented by luciferase reporter assay. Moreover, miR-6869-5p promoted M2 macrophage polarization and thus restrain inflammation. Accordingly, miR-6869-5p is involved in maintaining placental microenvironment balance by preventing from inflammation and inducing M2 macrophages in gestational diabetes mellitus.

摘要

在过去的十年中,miRNA(microRNA)在妊娠糖尿病中的作用得到了广泛研究。然而,miR-6869-5p 对妊娠糖尿病中免疫和胎盘微环境的改变作用在很大程度上尚不清楚。在我们的研究中,miR-6869-5p 的表达在胎盘衍生的单核巨噬细胞中被记录为显著降低,这也与 PTPRO 呈负相关。此外,PTPRO 被胎盘衍生的单核巨噬细胞中的 miR-6869-5p 负调控。在体外,miR-6869-5p 通过 EdU 和 CCK-8 实验抑制巨噬细胞增殖。miR-6869-5p 还显著抑制巨噬细胞的炎症反应,这可以通过荧光素酶报告基因实验来调节 PTPRO 作为一个靶点。此外,miR-6869-5p 促进 M2 巨噬细胞极化,从而抑制炎症。因此,miR-6869-5p 通过防止炎症和诱导妊娠糖尿病中的 M2 巨噬细胞参与维持胎盘微环境平衡。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/320e/8110425/d5faf993b47d/MI2021-6696636.001.jpg

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