Delayed implantation site development and impaired decidual angiogenesis via VEGF-KDR system disruption during mouse gastrulation following perigestational alcohol ingestion

BARRIL C; GUALDONI GS; JACOBO PV; SOBARZO CMA; CEBRAL E

Bogotá

Congreso; IX SLIMP MEETING VIRTUAL 2022: 9th Latin American Symposium on Maternal-Fetal Interaction and Placenta: "Placenta ephemeral: but leaving an important and lasting imprint".; 2022

Objectives: Perigestational alcohol consumption up to organogenesisproduces embryo growth restriction and defective maternal vascularization by reduced uNKs and VEGF expression.We aimed to determine whether perigestational alcohol intake up togastrulation produces early delayed growth of implantation sites (IS) andearlier alters decidual angiogenesis, uNK cell populations, and VEGF-KDRMMP-9 system.Methods. Ethanol 10% was administered to female mice (TF) for 17 daysbefore and up to days 8 and 8.5 of gestation. Free-ethanol water wasadministered to control females (CF). Histology (H-E, PAS), DBA-histochemistry, immunohistochemistry (IHC), immunofluorescence (IF),TUNEL, and morphometry (ImageJ) were performed in D8-8.5-IS toanalyze the vascular decidual tissue.Results. In TF, the percentage of delayed IS (TS10a+ab) increased whileadvanced IS (TS10b+TS11, Theiler Scale) diminished at D8-8.5 vs CFs. Withhistological alterations (H-E) and low extracellular matrix deposition(PAS), TF-IS area decreased in TS10b stage and at D8 vs CF-IS. Expansion ofdecidual vascular lumen/IS area was reduced in D8.5-IS from TF vs CF(p