Perigestational alcohol consumption induces altered early placentation and organogenic embryo growth restriction by disruption of trophoblast angiogenic factors

Research question Maternal alcohol consumption produces fetal retardation and malformations, probably associated with placental defects. Does perigestational up to organogenesis lead abnormal placentation embryo growth restriction by disrupting the vascular endothelial factor (VEGF) system in embryo–placental development? Design Female mice were treated 10% ethanol drinking water before day 10 of gestation. Control received ethanol-free water. After treatment, trophoblastic tissue, angiogenic VEGF pathway analysed. Results who had treatment resorbed delayed implantation sites poor ectoplacental cone development. Reduced area tissue from female junctional zone diminished labyrinthine vascularization. labyrinth increased chorionic trophoblast proliferation, hypoxia inducible factor-1? immunoexpression but reduced apoptosis. The was concomitantly low immunostaining high nitric oxide synthase (eNOS) expression. In mice, gene protein expression FLT-1 compared controls. Increased activation kinase insert domain receptor (phosphorylated KDR) eNOS observed placenta mice. Immunoexpression metalloproteinase-9, however, labyrinth, Conclusions These data reveal inadequate VEGF/receptors metalloproteinase factors related early after ingestion, providing insight into aetiological underlying placentopathy intrauterine caused maternal consumption.