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MiR-6869-5p Induces M2 Polarization by Regulating PTPRO in Gestational Diabetes Mellitus
Pingping Wang1, Zhenzhi Ma2, Zengyan Wang3
1Department of Gynecology and Obstetrics, the Affiliated Hospital of Maternal and Child Health, Weifang Medical University, Weifang 261000, China.
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.
Insights
MicroRNA-6869-5p (miR-6869-5p) is decreased in gestational diabetes mellitus, inhibiting macrophage inflammation and promoting M2 polarization to maintain placental health.
Area of Science:
- Immunology
- Reproductive Biology
- Molecular Biology
Background:
- Gestational diabetes mellitus (GDM) research has focused on microRNAs (miRNAs).
- The specific role of miR-6869-5p in GDM's impact on immunity and the placental microenvironment remains unclear.
- Understanding miRNA involvement is crucial for GDM pathogenesis.
Purpose of the Study:
- To investigate the function of miR-6869-5p in gestational diabetes mellitus.
- To determine miR-6869-5p's effect on macrophage immunity and placental microenvironment.
- To elucidate the regulatory relationship between miR-6869-5p and PTPRO in GDM.
Main Methods:
- Quantification of miR-6869-5p expression in placenta-derived macrophages.
- In vitro experiments assessing macrophage proliferation (EdU, CCK-8) and inflammatory response.
- Luciferase reporter assay to confirm PTPRO as a miR-6869-5p target.
- Analysis of M2 macrophage polarization.
Main Results:
- miR-6869-5p expression was significantly reduced in GDM placental macrophages and negatively correlated with PTPRO.
- miR-6869-5p inhibited macrophage proliferation and inflammatory cytokine production.
- miR-6869-5p directly targets and negatively regulates PTPRO.
- miR-6869-5p promoted M2 macrophage polarization, reducing inflammation.
Conclusions:
- miR-6869-5p plays a protective role in gestational diabetes mellitus.
- It maintains placental microenvironment balance by suppressing inflammation and inducing M2 macrophages.
- This miRNA represents a potential therapeutic target for GDM.
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