MiR-432-5p was involved in gestational diabetes mellitus by targeting COL5A2 regulation.

Ir J Med Sci

Department of Obstetrics and Gynecology, The People's Hospital of Yubei District of Chongqing, No.23, Central Park North Road, Chongqing, 401120, China.

Published: August 2025


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Article Abstract

Background: The prevalence of gestational diabetes mellitus (GDM) has increased recently. Currently, there is no effective treatment method, so this study aims to find a new biomarker for GDM.

Methods: MiR-432-5p expression and diagnostic value were detected in GDM by RT-qPCR and the receiver operating characteristic (ROC) curve. The correlation was analyzed utilizing Pearson correlation analysis. Logistic regression was utilized to analyze risk factors for GDM. To construct the GDM mouse model, female mice were fed a 45% kcal high-fat sucrose diet six weeks before mating to induce diabetes. MiR-432-5p was overexpressed and inhibited by injecting miR-432-5p agomir and miR-432-5p antagomir into the mice, and collagen type V alpha 2 chain (COL5A2) was overexpressed by injecting COL5A2 overexpression vectors into the mice.

Results: In GDM, miR-432-5p decreased and had high diagnostic value, and miR-432-5p was a risk factor. In GDM, miR-432-5p was negatively correlated with fasting plasma glucose, 1 h plasma glucose, and 2 h plasma glucose. In the GDM mouse model, overexpressed miR-432-5p reduced the fasting plasma glucose and body weight, while inhibited miR-432-5p increased them. Overexpressed miR-432-5p decreased the proliferation and increased the apoptosis in the GDM mouse model, while inhibited miR-432-5p increased the proliferation and decreased the apoptosis. COL5A2 was negatively regulated by miR-432-5p in GDM. Overexpressed COL5A2 increased the proliferation and reduced the apoptosis in the GDM mouse model.

Conclusion: In GDM, miR-432-5p decreased and might be a biomarker. COL5A2 was decreased and negatively correlated with miR-432-5p in GDM. MiR-432-5p and COL5A2 acted together on GDM.

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http://dx.doi.org/10.1007/s11845-025-04059-3DOI Listing

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