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MiR-6869-5p Induces M2 Polarization by Regulating PTPRO in Gestational Diabetes Mellitus
Author(s) -
Pingping Wang,
Zhenzhi Ma,
Zengyan Wang,
Ximei Wang,
Guifeng Zhao,
Zengfang Wang
Publication year - 2021
Publication title -
mediators of inflammation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.37
H-Index - 97
eISSN - 1466-1861
pISSN - 0962-9351
DOI - 10.1155/2021/6696636
Subject(s) - gestational diabetes , inflammation , macrophage polarization , placenta , microrna , diabetes mellitus , macrophage , immunology , peripheral blood mononuclear cell , m2 macrophage , biology , trophoblast , in vitro , medicine , endocrinology , pregnancy , gestation , fetus , biochemistry , gene , genetics
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.

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