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. 2019 Oct 25;14(1):119.
doi: 10.1186/s13000-019-0899-9.

miR-132 serves as a diagnostic biomarker in gestational diabetes mellitus and its regulatory effect on trophoblast cell viability

Xuegui Zhou  1 , Cuiping Xiang  2 , Xiaoxia Zheng  3
Affiliations

miR-132 serves as a diagnostic biomarker in gestational diabetes mellitus and its regulatory effect on trophoblast cell viability

Xuegui Zhou et al. Diagn Pathol. .

Abstract

Background: Gestational diabetes mellitus (GDM) leads to poor pregnancy outcomes. Strategies that improve trophoblast cell function are important methods for GDM treatment. This study aimed to investigate the expression and diagnostic potential of microRNA-132 (miR-132) in GDM patients, and further analyzed the effects of miR-132 on HTR-8/SVneo cell proliferation.

Methods: Quantitative real-time PCR was applied to estimate the expression of miR-132. A receiver operating characteristics curve (ROC) analysis was performed to evaluate the diagnostic value of serum miR-132 in GDM patients. In vitro regulation of miR-132 in trophoblast cell HTR-8/SVneo was achieved by cell transfection, and the effects of miR-132 on cell proliferation were assessed using CCK-8 assay.

Results: Expression of miR-132 was decreased in serum and placenta tissues in GDM patients compared with the healthy women. A negative correlation was found between the serum miR-132 levels and fasting blood glucose of the GDM patients. A ROC curve shown the serum miR-132 had considerable diagnostic accuracy with an area under the curve (AUC) of 0.898. High glucose (HG) treatment induced an inhibition in HTR-8/SVneo cell proliferation and the expression of miR-132. The overexpression of miR-132 in HTR-8/SVneo cells could markedly rescued the HG - induced suppressed cell proliferation.

Conclusion: All the data of this study revealed the reduced expression of miR-132 in serum and placenta tissues of GDM, and serum miR-132 serves a candidate biomarker in the diagnosis of GDM. miR-132 may act a protective role against GDM via enhancing the trophoblast cell proliferation.

Keywords: Diagnosis; Gestational diabetes mellitus; MicroRNA-132; Proliferation; Trophoblast cell.

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Conflict of interest statement

The authors declare that they have no competing interests.

Figures

Fig. 1
Fig. 1
Expression of miR-132 and its correlation with fasting blood glucose in patients with GDM. a and b. Expression of miR-132 in serum (a) and placenta tissue (b) was downregulated in GDM patients compared with the healthy women. c. Serum miR-132 levels were negatively correlated with the fasting blood glucose of the GDM patients (r = − 0.490, P < 0.001). ***P < 0.001
Fig. 2
Fig. 2
A ROC curve based on serum miR-132 in GDM patients. The area under the curve (AUC) was 0.898 for serum miR-132 expression to distinguish GDM cases from healthy pregnant women
Fig. 3
Fig. 3
HG suppressed cell proliferation (a) and inhibited the expression of miR-132 (b) in two trophoblast cell lines HTR-8/SVneo and BeWo. HG, high glucose; *P < 0.05, **P < 0.01, ***P < 0.001
Fig. 4
Fig. 4
Effects of miR-132 on cell proliferation of trophoblast cells upon HG treatment. a. Expression of miR-132 was upregulated by the miR-132 mimic, but was downregulated by the miR-132 inhibitor in both HTR-8/SVneo and BeWo cell lines. b. The upregulation of miR-132 promoted cell proliferation, while the downregulation of miR-132 inhibited cell proliferation in HTR-8/SVneo and BeWo cells. HG, high glucose; *P < 0.05, **P < 0.01, ***P < 0.001
See this image and copyright information in PMC

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