Academic Seminars

“Preeclampsia: New Insights for the Mechanisms of Vascular Endothelial Dysfunction” presented by Sandra Davidge, Ph.D.
October 4, 2016
 

Sandra Davidge, Ph.D., Professor, Dept of OB/GYN and Physiology, University of Alberta, Director Women and Children Health Res Inst, Canada Research Chair in Maternal and Perinatal CV Health. Presented October 7, 11:00-12:00, LIB-110.
Synopsis: Preeclampsia, defined as new-onset hypertension with proteinuria after 20 weeks of gestation, is a leading cause of maternal and perinatal morbidity and mortality. Systemic maternal vascular dysfunction is a major phenotype of pregnancies with preeclampsia contributing to increased peripheral vascular resistance, maternal hypertension, and proteinuria. The mechanisms of systemic vascular dysfunction in preeclamptic pregnancies includes impaired endothelial-dependent vascular relaxation and oxidative stress. However, the cause of preeclampsia is currently unknown. A number of circulating factors have been implicated to cause vascular dysfunction including those of placental origin, thus providing a link between placental and maternal vascular dysfunction. We have been exploring the role of placental extracellular vesicles (STBEVs) in maternal vascular dysfunction. We propose that they contribute to endothelial dysfunction by activating the lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) receptor. We hypothesize that circulating factors, and specifically STBEVs, induce endothelial dysfunction via LOX-1 by increasing superoxide production, which leads to a decreased nitric oxide bioavailability. Overall, the studies described are providing fundamental insights into the vascular pathophysiology of preeclampsia.