IFIBIO HOUSSAY   25014
INSTITUTO DE FISIOLOGIA Y BIOFISICA BERNARDO HOUSSAY
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
BRAIN MICROVASCULAR ENDOTHELIAL RESPONSE TO STIMULI FROM THE PLACENTA. PRELIMINARY RESULTS
Autor/es:
REPPETTI, JULIETA; TRONCOSO, FELIPE; ESCUDERO, CARLOS; ACURIO JESENIA ; DAMIANO, ALICIA E; LEÓN, JOSÉ; MARTINEZ, NORA
Reunión:
Congreso; III Meeting on Research and Innovation in Vascular Health; V Meeting on Hypertension in Pregnancy; 2019
Institución organizadora:
Grivas Health
Resumen:
BackgroundPathophysiology of brain damage in preeclampsia is unclear. But, current hypothesis indicates that hypoxia/reoxygenation induces placental damage that enhances shedding of syncytiotrophoblast microparticles including apoptotic bodies or exosomes into maternal circulation causing brain microvascular endothelium dysfunction. Also, emerging evidence suggests that an intact caveola is necessary for adequate endothelial cell function. Caveola is a small uncoated pit found in the cell membrane of many highly differentiated mammalian cells including endothelium. Within the caveola increasing number of signaling proteins have been documented, including Caveolin-1 (Cav-1) and aquaporin 1 and 4 (AQP1, AQP4) which normal function is related to cell migration and vascular permeability.AimsTo evaluate whether conditioned media from placentas exposed to hypoxia/reoxygenation impairs brain endothelial cells migration and expression of Cav-1, AQP1, AQP4.MethodsHuman brain microvascular cell line hCMEC/D3 was exposed (24 h) to conditionedmedium (CM) harvested from normal pregnancy placentas explants cultured in: a) N: normoxia (20% O 2 ); b) H: hypoxia (2% O 2 ); and c) H/R: hypoxia/reoxygenation. Caveolin-1 (Cav-1), aquaporin 1 and 4 (AQP1, AQP4) expressions were evaluated by RT-PCR and Western Blot. To evaluate the role of Cav-1, methyl-β-cyclodextrin (MβCD-5 mM, 30 min) was used to disrupt the caveolae and then hCMEC/D3 migration was evaluated by the wound healing assay (0 to 20 h).ResultsCM from hypoxic placentas significantly increased hCMEC/D3 cell migration at 6h and 8h (n=3; p