Funding outcome

Preeclampsia (PE) is a prevalent threat to maternal and fetal health affecting ~5% of pregnancies in Canada, characterized by high blood pressure (hypertension) and adverse pregnancy outcomes. PE is a significant threat to public health, as it is a major cause of morbidity and mortality for both the mother and the child, and negatively impacts their cardiovascular health later in life. To date, the only known cure is the removal of the placenta. A potential factor that may cause hypertension in PE is impaired function of the mother's blood vessels, specifically the endothelial cells, which line the inner walls of blood vessels and regulate vessel function. Impaired function of endothelial cells results in blood vessel dysfunction, which may ultimately lead to elevated blood pressure. A normal placenta releases cellular particles into the maternal bloodstream. It is thought that women with PE have an abnormal placenta and that elevated release of these particles may impair endothelial function. However, the impact of placental particles from PE on endothelial function has yet to be explored. Thus, we aimed to study if, and how, placental particles from PE pregnancies impact endothelial function compared to placental particles from normal pregnancies. Using endothelial cells from human umbilical cords, we will evaluate the mechanisms and the effects of placental particles isolated from normal or PE placentas on endothelial function. This research will further our understanding of the role the placenta may play in the development of PE and enable us to develop new therapies to prevent or reduce the adverse outcomes of PE.