AI Article Synopsis
- Children born to mothers with gestational diabetes mellitus (GDM) face a higher risk of developing health issues like hypertension, type 2 diabetes, and obesity due to changes in their endothelial colony-forming cells (ECFCs).
- ECFCs from GDM pregnancies showed increased proliferation but had a diminished ability to form networks in Matrigel, indicating altered functionality when compared to control ECFCs.
- The study found that GDM-exposed ECFCs are resistant to the adverse effects of hyperglycemia, as they do not activate the p38MAPK pathway like control ECFCs, suggesting they have adapted to better tolerate high glucose environments.
Article Abstract
Background: Children born to mothers with gestational diabetes mellitus (GDM) experience increased risk of developing hypertension, type 2 diabetes mellitus, and obesity. Disrupted function of endothelial colony-forming cells (ECFCs) may contribute to this enhanced risk. The goal of this study was to determine whether cord blood ECFCs from GDM pregnancies exhibit altered functionality.
Methods: ECFCs isolated from the cord blood of control and GDM pregnancies were assessed for proliferation, senescence, and Matrigel network formation. The requirement for p38MAPK in hyperglycemia-induced senescence was determined using inhibition and overexpression studies.
Results: GDM-exposed ECFCs were more proliferative than control ECFCs. However, GDM-exposed ECFCs exhibited decreased network-forming ability in Matrigel. Aging of ECFCs by serial passaging led to increased senescence and reduced proliferation of GDM-exposed ECFCs. ECFCs from GDM pregnancies were resistant to hyperglycemia-induced senescence compared with those from controls. In response to hyperglycemia, control ECFCs activated p38MAPK, which was required for hyperglycemia-induced senescence. In contrast, GDM-exposed ECFCs showed no change in p38MAPK activation under equivalent conditions.
Conclusion: Intrauterine exposure of ECFCs to GDM induces unique phenotypic alterations. The resistance of GDM-exposed ECFCs to hyperglycemia-induced senescence and decreased p38MAPK activation suggest that these progenitor cells have undergone changes that induce tolerance to a hyperglycemic environment.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3944713 | PMC |
| http://dx.doi.org/10.1038/pr.2013.224 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Engineering bioactive nanoparticles to rejuvenate vascular progenitor cells.
Commun Biol
June 2022
Department of Aerospace and Mechanical Engineering, Bioengineering Graduate Program, University of Notre Dame, Notre Dame, IN, 46556, USA.
Fetal exposure to gestational diabetes mellitus (GDM) predisposes children to future health complications including type-2 diabetes mellitus, hypertension, and cardiovascular disease. A key mechanism by which these complications occur is through stress-induced dysfunction of endothelial progenitor cells (EPCs), including endothelial colony-forming cells (ECFCs). Although several approaches have been previously explored to restore endothelial function, their widespread adoption remains tampered by systemic side effects of adjuvant drugs and unintended immune response of gene therapies.
View Article and Find Full Text PDFTransgelin induces dysfunction of fetal endothelial colony-forming cells from gestational diabetic pregnancies.
Am J Physiol Cell Physiol
October 2018
Department of Cellular and Integrative Physiology, Indiana University School of Medicine, Indianapolis, Indiana.
Fetal exposure to gestational diabetes mellitus (GDM) predisposes children to future health complications including hypertension and cardiovascular disease. A key mechanism by which these complications occur is through the functional impairment of vascular progenitor cells, including endothelial colony-forming cells (ECFCs). Previously, we showed that fetal ECFCs exposed to GDM have decreased vasculogenic potential and altered gene expression.
View Article and Find Full Text PDFEpigenetic Regulation of Placenta-Specific 8 Contributes to Altered Function of Endothelial Colony-Forming Cells Exposed to Intrauterine Gestational Diabetes Mellitus.
Diabetes
July 2015
Department of Pediatrics, Indiana University School of Medicine, Indianapolis, IN Herman B Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN Department of Cellular and Integrative Physiology, Indiana University School of Medicine, Indianapolis, IN Department of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, IN Indiana University Melvin and Bren Simon Cancer Center, Indiana University School of Medicine, Indianapolis, IN
Intrauterine exposure to gestational diabetes mellitus (GDM) is linked to development of hypertension, obesity, and type 2 diabetes in children. Our previous studies determined that endothelial colony-forming cells (ECFCs) from neonates exposed to GDM exhibit impaired function. The current goals were to identify aberrantly expressed genes that contribute to impaired function of GDM-exposed ECFCs and to evaluate for evidence of altered epigenetic regulation of gene expression.
View Article and Find Full Text PDFGestational diabetes induces alterations in the function of neonatal endothelial colony-forming cells.
Pediatr Res
February 2014
1] 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 [3] Indiana University Simon Cancer Center, Indiana University School of Medicine, Indianapolis, Indiana [4] Department of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, Indiana [5] Department of Cellular and Integrative Physiology, Indiana University School of Medicine, Indianapolis, Indiana.
Article Synopsis
- Children born to mothers with gestational diabetes mellitus (GDM) face a higher risk of developing health issues like hypertension, type 2 diabetes, and obesity due to changes in their endothelial colony-forming cells (ECFCs).
- ECFCs from GDM pregnancies showed increased proliferation but had a diminished ability to form networks in Matrigel, indicating altered functionality when compared to control ECFCs.
- The study found that GDM-exposed ECFCs are resistant to the adverse effects of hyperglycemia, as they do not activate the p38MAPK pathway like control ECFCs, suggesting they have adapted to better tolerate high glucose environments.
Want AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!