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

dc.contributor.authorBlue, Emily K.
dc.contributor.authorDiGiuseppe, Robert
dc.contributor.authorDerr-Yellin, Ethel
dc.contributor.authorAcosta, Juan Carlos
dc.contributor.authorPay, S. Louise
dc.contributor.authorHanenberg, Helmut
dc.contributor.authorSchellinger, Megan M.
dc.contributor.authorQuinney, Sara K.
dc.contributor.authorMund, Julie A.
dc.contributor.authorCase, Jamie
dc.contributor.authorHaneline, Laura S.
dc.contributor.departmentPediatrics, School of Medicine
dc.date.accessioned2025-04-28T08:06:55Z
dc.date.available2025-04-28T08:06:55Z
dc.date.issued2014
dc.description.abstractBackground: 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.versionAuthor's manuscript
dc.identifier.citationBlue 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.urihttps://hdl.handle.net/1805/47493
dc.language.isoen_US
dc.publisherSpringer Nature
dc.relation.isversionof10.1038/pr.2013.224
dc.relation.journalPediatric Research
dc.rightsPublisher Policy
dc.sourcePMC
dc.subjectCollagen
dc.subjectFetal blood
dc.subjectHyperglycemia
dc.subjectEndothelial cells
dc.titleGestational diabetes induces alterations in the function of neonatal endothelial colony forming cells
dc.typeArticle
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