Researcher to study causes of complications in pregnancy
Oct. 25, 2013 College News - The Medical College of Wisconsin (MCW) and the Children’s Hospital of Wisconsin Research Institute have received a four year, $1.5 million grant from the National Institutes of Health’s National Heart, Lung and Blood Institute to study abnormalities in blood coagulation that affect women’s health and pregnancy. The grant will specifically focus on the role of maternal platelets in the placenta and pregnancy complications. Placenta-mediated pregnancy complications have serious health consequences for the mother and the baby.
Rashmi Sood, PhD, Assistant Professor of Pathology at MCW and an investigator at the Research Institute, is the primary investigator of this grant. Her research is focused on studying how environmental pollution and preexisting maternal conditions, such as thrombophilia, diabetes and obesity, compromise placental function. Suboptimal placental function is associated with fetal growth restriction, small birth weight, preterm delivery and, in severe cases, fetal or perinatal death. It increases the risk of diabetes and cardiovascular disease in adult life. Adverse consequences for the mother include hypertensive disorders, such as preeclampsia. These conditions affect 5 to 8% of all pregnancies.
A developing fetus relies on the placenta for nutrition and other essential functions. To perform these functions, the human placenta forms unusual vascular spaces filled with maternal blood and directly accessible to placental cells. Such vascular spaces are not found anywhere else in the human body. It is unclear how blood flow is maintained in these vascular spaces and how blood clotting abnormalities (thrombophilias) compromise placental function.
Using rodent models of blood clotting abnormalities, the Sood laboratory has established a critical and unconventional role of maternal platelets in causing thrombophilia-associated placental dysfunction and fetal death. The federal grant has been awarded to examine the mechanisms by which maternal platelets cause placental abnormality. Understanding these mechanisms is expected to improve our ability to identify targets of therapeutic intervention for reducing or preventing thrombophilia-associated placental disease.