Characterisation of molecular and phenotypic effects induced by Gestational Diabetes Mellitus (GDM) on endothelial cells and placenta tissue
TL;DRAbstract
Gestational diabetes mellitus (GDM) is characterised by maternal hyperglyceamia first recognised during pregnancy. GDM produces chronic foetal hyperglyceamia and expressional changes in foetal endothelial cells (ECs). \n<br>Epigenetic modulation of foetal endothelial genes by the intra-uterine environment has been proposed. MicroRNAs (miRs) inhibit the expression of their mRNA targets and have been implicated in diabetes-induced endothelial dysfunction. MiR-101 impairs EC in part via direct inhibition of the methyltransferase Enhancer of Zester Homolog2 (EZH2) which catalysed the trimethylation on lysine 27 of histone H3 (H3K27m3).</br> \nWe aimed to characterize the molecular and functional impact of GDM on the foetal ECs derived from the umbilical cord vein (HUVECs). \n<br>HUVECs prepared from GDM or healthy pregnancies, were assessed for apoptosis, migration, and angiogenic capacity. GDM-HUVECs showed decreased functional capacities, increased miR-101,
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Gestational diabetes mellitus (GDM) is characterised by maternal hyperglyceamia first recognised during pregnancy. GDM produces chronic foetal hyperglyceamia and expressional changes in foetal endothelial cells (ECs). \n<br>Epigenetic modulation of foetal endothelial genes by the intra-uterine environment has been proposed. MicroRNAs (miRs) inhibit the expression of their mRNA targets and have been implicated in diabetes-induced endothelial dysfunction. MiR-101 impairs EC in part via direct inhibition of the methyltransferase Enhancer of Zester Homolog2 (EZH2) which catalysed the trimethylation on lysine 27 of histone H3 (H3K27m3).</br> \nWe aimed to characterize the molecular and functional impact of GDM on the foetal ECs derived from the umbilical cord vein (HUVECs). \n<br>HUVECs prepared from GDM or healthy pregnancies, were assessed for apoptosis, migration, and angiogenic capacity. GDM-HUVECs showed decreased functional capacities, increased miR-101,
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