BECAS
REPPETTI Julieta
congresos y reuniones científicas
Título:
IMPACT OF HYPEROSMOLARITY ON PLACENTAL ANGIOGENESIS AND CAVEOLIN-1 EXPRESSION
Autor/es:
REPPETTI J.; GORNALUSSE G.; BELTRAMONE N.; DAMIANO A. E.; MARTINEZ N.
Reunión:
Congreso; REUNION ANUAL DE LA SOCIEDAD ARGENTINA DE FISIOLOGIA; 2023
Resumen:
IMPACT OF HYPEROSMOLARITY ON PLACENTAL ANGIOGENESIS AND CAVEOLIN-1 EXPRESSIONReppetti J1, Gornalusse G2, Beltramone N3, Damiano AE1,4, Martinez N11.Laboratorio de Biología de la Reproducción. IFIBIO-Houssay (UBA-CONICET). Facultad de Medicina, Universidad de Buenos Aires. Buenos Aires, Argentina.2.Department of Medicine, University of Washington, Seattle, Washington, USA.3.IFIBIO-Houssay (UBA-CONICET). Facultad de Medicina, Universidad de Buenos Aires. Buenos Aires, Argentina.4.Cátedra de Biología Celular y Molecular. Departamento de Ciencias Biológicas, Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, Buenos Aires, Argentina.Introduction:The establishment of a successful pregnancy requires proper development of placental vasculature, which includes macrovasculature and microvasculature, and the coordinated regulation of vascular processes. In this context, the placenta can act as a sensor of fetal metabolic demands, inducing changes in its vasculature to ensure fetal growth and well-being. Cellular stress during pregnancy, including hyperosmolar stress, can impact the normal development of placental vasculature. Caveolin-1 (Cav-1), a constitutive protein of caveolae, plays a pivotal role in cell signaling. Our hypothesis is that hyperosmolar stress disrupts placental angiogenesis, and Cav-1 participates in this process.Objective:Our objective was to assess the effect of hyperosmolarity on placental migration and tubulogenesis, along with the expression of Cav-1 under these conditions.Materials and Methods:This study received approval from the ethics committee of the Hospital Nacional Prof. Dr. A. Posadas. Placental microvascular endothelial cells (hPMEC) and the EA.hy926 cell line (ATCC® CRL-2922™) were used. Cells were treated with a sucrose solution (150 mM) to induce hyperosmolarity. Cav-1 expression was evaluated through RT-qPCR and western blot analysis. Cell migration was assessed via wound healing assays, and angiogenesis was evaluated through tube formation assays.Results:Hyperosmolar stress significantly reduced cell migration (p