Preeclampsia is a devastating hypertensive disorder of pregnancy that impacts 5-10% of pregnancies and causes significant maternal-fetal morbidity and mortality. Unfortunately, the only available treatment for preeclampsia at present is delivery of the baby and placenta. This often results in premature delivery, which is also associated with significant risks to mother and baby. To better understand potential therapeutic targets for the treatment of preeclampsia, I am working to understand how serotonin dysregulation interrupts immune and vascular function in the context of the disease. Serotonin is a neurotransmitter that, in addition to many central nervous system functions, also regulates vascular tone and blood platelet aggregation. To determine the role of serotonin dysregulation in preeclampsia, we are investigating serotonin dysregulation in an animal model of preeclampsia, as well as in clinical samples taken from women who experienced preeclampsia during pregnancy. We will use pharmacological and genetic manipulations to isolate particular targets of serotonin (e.g., receptors, downstream effectors, immune signaling molecules) that are disrupted in the context of preeclampsia, and determine whether targeting these factors might rescue immunovascular disease phenotypes. Collectively, it is our hope that these studies will indicate both targets for potential preeclampsia therapeutics, as well as biomarkers for improved detection of this often debilitating condition.