Differential Expression of miR-136 in Gestational Diabetes Mellitus Mediates the High-Glucose-Induced Trophoblast Cell Injury through Targeting E2F1

Abstract EN

Background.

Gestational diabetes mellitus (GDM) seriously affects the health of mothers and infants.

The high-glucose-induced inhibition in trophoblast cell viability is an important event in GDM pathogenesis.

This study evaluated the expression and clinical significance of miR-136 in GDM patients, and the biological function and related mechanisms of miR-136 in the regulation of trophoblast cell proliferation were explored.

Methods.

The expression of miR-136 in serum and placenta of GDM patients was measured using quantitative Real-Time PCR.

Trophoblast cells were stimulated with high-glucose medium to mimic the pathological changes of GDM, and the effect of miR-136 was examined by CCK-8 assay.

A luciferase reporter assay was used to confirm the target gene of miR-136, and the relationship of E2F transcription factor 1 (E2F1) with miR-136 in GDM was further analyzed.

Results.

miR-136 expression was significantly elevated in GDM serum and tissue samples.

By high-glucose treatment, trophoblast cell proliferation was inhibited and miR-136 expression was promoted.

The knockdown of miR-136 could promote the proliferation of trophoblast cells exposed to high glucose, whereas the overexpression of miR-136 could suppress it.

In addition, E2F1 was identified as a target gene of miR-136, which could mediate the regulatory effect of miR-136 on trophoblast cell proliferation.

Conclusion.

Collectively, miR-136 expression is increased in both serum and placental tissues in GDM patients, and miR-136 mediates the inhibiting effect of high glucose on trophoblast cell viability by targeting E2F1.