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

Pingping Wang,Zengyan Wang,Ximei Wang,Zhenzhi Ma,Guifeng Zhao,Zengfang Wang,Jie Chen

doi:10.1155/2021/6696636

Pingping Wang, Zengyan Wang + Show 5 more

Open Access

https://doi.org/10.1155/2021/6696636

Copy DOI

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.

Highlights

Gestational diabetes mellitus is a common complication in pregnant females, who usually have normal glucose metabolism or potential abnormal glucose tolerance [1]
Increased expression of phosphatase receptor type O (PTPRO) was found in placenta-derived macrophages from patients with gestational diabetes mellitus (Figure 1(b))
We hypothesize that miR-6869-5p might regulate macrophage polarization in placental immune microenvironment and induces macrophages towards M2 polarization in gestational diabetes mellitus

Summary

Introduction

Gestational diabetes mellitus is a common complication in pregnant females, who usually have normal glucose metabolism or potential abnormal glucose tolerance [1]. The incidence of gestational diabetes mellitus has been increasing during the past few decades. Most patients with gestational diabetes mellitus can return to normal glucose metabolism postpartumly, but they are at an elevated risk of developing type II diabetes in the future. The pathogenesis of gestational diabetes mellitus is unclear yet. Abnormal glucose metabolism during gestation can cause pregnancy failure, dystocia, stillbirth, fetal death, and fetal macrosomia increased owing to complicated factors [2]. Identifying useful way for gestational diabetes mellitus prevention and treatment is urgent

Objectives

Methods

Results

Conclusion