Background <p>Gestational diabetes mellitus (GDM) causes APOs. The diagnostic OGTT has a lag, and the role of lncRNA EGFR-AS1 in GDM has potential.</p> Aims <p>This study evaluated the potential of EGFR-AS1 for the GDM clinical application and explored the role of the EGFR-AS1/miR-142-5p/ROCK2 axis in placental endothelial injury.</p> Methods <p>Serum EGFR-AS1, miR-142-5p and ROCK2 levels were detected via qPCR in 135 GDM patients and 110 healthy pregnant women. The clinic value of EGFR-AS1 was analyzed using ROC and logistic regression. A high glucose (HG)-induced model was established, in which EGFR-AS1 was silenced alone or co-silenced with miR-142-5p. The regulatory mechanism of EGFR-AS1/miR-142-5p/ROCK2 axis on placental endothelial injury was then analyzed via CCK-8, ELISA, qPCR, and WB.</p> Results <p>In GDM patients, serum EGFR-AS1 and ROCK2 were elevated, whereas miR-142-5p was reduced. Serum EGFR-AS1 showed high diagnostic efficiency for GDM and acted as an independent predictor of APOs occurrence. Silencing EGFR-AS1 reversed HG-induced HPVECs injury—evidenced by inhibited inflammatory factor release, balanced oxidative stress, up-regulated pro-angiogenic factors mRNA expression, and down-regulated proteins expression related to apoptosis and endothelial injury. Dual-luciferase reporter assays confirmed binding between EGFR-AS1 and miR-142-5p, as well as between miR-142-5p and ROCK2. Notably, co-inhibiting EGFR-AS1 and miR-142-5p abolished the protective effect of EGFR-AS1 silencing.</p> Conclusions <p>EGFR-AS1 is a clinical auxiliary biomarker for GDM diagnosis and prediction. It aggravates HPVECs injury via EGFR-AS1/miR-142-5p/ROCK2 axis, which impairs placental function and triggers APOs, providing a new target for GDM intervention.</p>

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Clinical significance of lncRNA EGFR-AS1 in gestational diabetes mellitus and its regulation of endothelial cell function

  • Hui Jiang,
  • Pengcheng Wu,
  • Min Zhang,
  • Congxiang Liu

摘要

Background

Gestational diabetes mellitus (GDM) causes APOs. The diagnostic OGTT has a lag, and the role of lncRNA EGFR-AS1 in GDM has potential.

Aims

This study evaluated the potential of EGFR-AS1 for the GDM clinical application and explored the role of the EGFR-AS1/miR-142-5p/ROCK2 axis in placental endothelial injury.

Methods

Serum EGFR-AS1, miR-142-5p and ROCK2 levels were detected via qPCR in 135 GDM patients and 110 healthy pregnant women. The clinic value of EGFR-AS1 was analyzed using ROC and logistic regression. A high glucose (HG)-induced model was established, in which EGFR-AS1 was silenced alone or co-silenced with miR-142-5p. The regulatory mechanism of EGFR-AS1/miR-142-5p/ROCK2 axis on placental endothelial injury was then analyzed via CCK-8, ELISA, qPCR, and WB.

Results

In GDM patients, serum EGFR-AS1 and ROCK2 were elevated, whereas miR-142-5p was reduced. Serum EGFR-AS1 showed high diagnostic efficiency for GDM and acted as an independent predictor of APOs occurrence. Silencing EGFR-AS1 reversed HG-induced HPVECs injury—evidenced by inhibited inflammatory factor release, balanced oxidative stress, up-regulated pro-angiogenic factors mRNA expression, and down-regulated proteins expression related to apoptosis and endothelial injury. Dual-luciferase reporter assays confirmed binding between EGFR-AS1 and miR-142-5p, as well as between miR-142-5p and ROCK2. Notably, co-inhibiting EGFR-AS1 and miR-142-5p abolished the protective effect of EGFR-AS1 silencing.

Conclusions

EGFR-AS1 is a clinical auxiliary biomarker for GDM diagnosis and prediction. It aggravates HPVECs injury via EGFR-AS1/miR-142-5p/ROCK2 axis, which impairs placental function and triggers APOs, providing a new target for GDM intervention.