Grant: Travel Awards - Institute Community Support

Preeclampsia (PE) is a vascular complication of pregnancy that is a leading cause of maternal disease and death worldwide. It is one of the most common reasons for induced preterm delivery. PE is diagnosed by the development of high blood pressure and kidney damage after the 20th week of gestation. Both the cause and course of the disease remain poorly understood and delivery of the placenta and fetus is currently the only known cure for PE. Nonetheless, there is substantial evidence that reduced blood vessel function contributes to the development of high blood pressure in the disease. It is believed that this might be due to small (toxic) particles that are released from the placenta into the mother's bloodstream. This could affect the function of the mother's blood vessels and contribute to the development of high blood pressure later in her pregnancy. However, the specific cause(s) and process(es) are not completely understood. The research in this abstract focuses on how the placental particles released from the placenta can affect the function of blood vessels. Our lab recently made the exciting discovery of a new pathway involving a receptor called LOX-1 that disrupts the normal function of blood vessels in women with PE. We used uterine arteries from mice and incubated them with the placental particles to measure the blood vessel function afterwards. We observed that the placental particles can help with the adaptations that blood vessels normally make during pregnancy to support normal development of the fetus. We also showed that the specific pathway via LOX-1 indeed appeared to be activated by the placental particles. This study further determined the role of the LOX-1 pathway and the role the placental particles play in this in the development of reduced blood vessel function in PE. This increased our understanding of the development of PE during pregnancy in order to develop new therapeutic strategies to treat this disorder in the future.