ArticlePediatric research2014
Gestational diabetes induces alterations in the function of neonatal endothelial colony-forming cells.
Article in Pediatric research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
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Who cites it
25 citing papers in PubMed, 42 citations in OpenAlex.
- An assessment of the functional state of endothelial colony forming cells from patients with diabetes mellitus and chronic limb threatening ischemia.Stem cells translational medicine · 2025Article
- The immunological age prediction of monocytes indicates that gestational diabetes mellitus accelerates the aging of monocytes in offspring.Immunity & ageing : I & A · 2025Article
- Human Cord Blood Endothelial Progenitor Cells and Pregnancy Complications (Preeclampsia, Gestational Diabetes Mellitus, and Fetal Growth Restriction).International journal of molecular sciences · 2024Review
- Recent advances in endothelial colony-forming cells: from the transcriptomic perspective.Journal of translational medicine · 2024Review
- Mitochondrial Dysfunction in Endothelial Progenitor Cells: Unraveling Insights from Vascular Endothelial Cells.Biology · 2024Review
- Enhancing endothelial colony-forming cells for treating diabetic vascular complications: challenges and clinical prospects.Frontiers in endocrinology · 2024Review
- Analysis of global DNA methylation and epigenetic modifiers (DNMTs and HDACs) in human foetal endothelium exposed to gestational and type 2 diabetes.Epigenetics · 2023Article
- Endothelial progenitor cells in pregnancy-related diseases.Clinical science (London, England : 1979) · 2023Review
- Increased circulating endothelial progenitor cells (EPCs) in prepubertal children born prematurely: a possible link between prematurity and cardiovascular risk.Pediatric research · 2021Article
- Bradykinin Protects Human Endothelial Progenitor Cells from High-Glucose-Induced Senescence through B2 Receptor-Mediated Activation of the Akt/eNOS Signalling Pathway.Journal of diabetes research · 2021Article
- Low Ethanol Concentrations Promote Endothelial Progenitor Cell Capacity and Reparative Function.Cardiovascular therapeutics · 2020Article
- β-3 adrenergic receptor gene polymorphisms are associated with gestational diabetes mellitus in a Chinese population.Medicine · 2019Article
- Maternal Gestational Diabetes Is Associated With Offspring's Hypertension.American journal of hypertension · 2019Article
- Transgelin induces dysfunction of fetal endothelial colony-forming cells from gestational diabetic pregnancies.American journal of physiology. Cell physiology · 2018Article
- Kinetic Analysis of Vasculogenesis Quantifies Dynamics of Vasculogenesis and Angiogenesis In Vitro.Journal of visualized experiments : JoVE · 2018Article
- From cord to caudate: characterizing umbilical cord blood stem cells and their paracrine interactions with the injured brain.Pediatric research · 2018Review
- Tissue regeneration using endothelial colony-forming cells: promising cells for vascular repair.Pediatric research · 2018Review
- Umbilical Cord Blood Circulating Progenitor Cells and Endothelial Colony-Forming Cells Are Decreased in Preeclampsia.Reproductive sciences (Thousand Oaks, Calif.) · 2017Article
- Pituitary adenylate cyclase-activating polypeptide attenuates tumor necrosis factor-α-induced apoptosis in endothelial colony-forming cells.Biomedical reports · 2017Article
- Mesenchyme Homeobox 2 Enhances Migration of Endothelial Colony Forming Cells Exposed to Intrauterine Diabetes Mellitus.Journal of cellular physiology · 2017Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundChildren 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.
methodsECFCs 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.
resultsGDM-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.
conclusionIntrauterine 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.
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