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Gestational diabetes induces alterations in the function of neonatal endothelial colony-forming cells

Emily K Blue1, Robert DiGiuseppe2, Ethel Derr-Yellin1

  • 11] Department of Pediatrics, Indiana University School of Medicine, Indianapolis, Indiana [2] Herman B Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, Indiana.

Pediatric Research
|November 16, 2013
PubMed

Insights

Gestational diabetes mellitus (GDM) alters fetal endothelial colony-forming cells (ECFCs), making them resistant to high glucose but impairing their network formation. This suggests GDM induces unique cellular adaptations in newborns.

Area of Science:

  • Vascular biology
  • Endothelial progenitor cell research
  • Maternal-fetal medicine

Background:

  • Children of mothers with gestational diabetes mellitus (GDM) face higher risks of hypertension, type 2 diabetes, and obesity.
  • Dysfunctional endothelial colony-forming cells (ECFCs) may underlie these increased risks.
  • This study investigates ECFC function in GDM pregnancies.

Purpose of the Study:

  • To determine if ECFCs from GDM pregnancies exhibit altered functionality.
  • To assess the impact of intrauterine GDM exposure on ECFC phenotype and behavior.

Main Methods:

  • ECFCs were isolated from cord blood of control and GDM pregnancies.
  • Assessed ECFCs for proliferation, senescence, and Matrigel network formation.
  • Investigated the role of p38MAPK in hyperglycemia-induced senescence via inhibition and overexpression.

Main Results:

  • GDM-ECFCs showed increased proliferation but decreased network formation.
  • GDM-ECFCs were resistant to hyperglycemia-induced senescence.
  • Control ECFCs activated p38MAPK in response to hyperglycemia, a pathway not activated in GDM-ECFCs.

Conclusions:

  • Intrauterine GDM exposure induces unique phenotypic alterations in ECFCs.
  • GDM-ECFCs exhibit resistance to hyperglycemia-induced senescence.
  • Decreased p38MAPK activation in GDM-ECFCs suggests adaptation to a hyperglycemic environment.
Abstract

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