Gestational diabetes induces alterations in the function of neonatal endothelial colony forming cells
dc.contributor.author | Blue, Emily K. | |
dc.contributor.author | DiGiuseppe, Robert | |
dc.contributor.author | Derr-Yellin, Ethel | |
dc.contributor.author | Acosta, Juan Carlos | |
dc.contributor.author | Pay, S. Louise | |
dc.contributor.author | Hanenberg, Helmut | |
dc.contributor.author | Schellinger, Megan M. | |
dc.contributor.author | Quinney, Sara K. | |
dc.contributor.author | Mund, Julie A. | |
dc.contributor.author | Case, Jamie | |
dc.contributor.author | Haneline, Laura S. | |
dc.contributor.department | Pediatrics, School of Medicine | |
dc.date.accessioned | 2025-04-28T08:06:55Z | |
dc.date.available | 2025-04-28T08:06:55Z | |
dc.date.issued | 2014 | |
dc.description.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. | |
dc.eprint.version | Author's manuscript | |
dc.identifier.citation | Blue EK, DiGiuseppe R, Derr-Yellin E, et al. Gestational diabetes induces alterations in the function of neonatal endothelial colony-forming cells. Pediatr Res. 2014;75(2):266-272. doi:10.1038/pr.2013.224 | |
dc.identifier.uri | https://hdl.handle.net/1805/47493 | |
dc.language.iso | en_US | |
dc.publisher | Springer Nature | |
dc.relation.isversionof | 10.1038/pr.2013.224 | |
dc.relation.journal | Pediatric Research | |
dc.rights | Publisher Policy | |
dc.source | PMC | |
dc.subject | Collagen | |
dc.subject | Fetal blood | |
dc.subject | Hyperglycemia | |
dc.subject | Endothelial cells | |
dc.title | Gestational diabetes induces alterations in the function of neonatal endothelial colony forming cells | |
dc.type | Article |