Discovering the mechanisms of abnormal blood vessel function in the pregnancy complication preeclampsia
Preeclampsia is a pregnancy-specific health complication characterized by the development of high blood pressure in the second half of pregnancy, and is one of the main causes of maternal sickness and death. Unfortunately, this condition impacts normal fetal growth and increases the risk for both the mother and her offspring to develop heart diseases later in life. Moreover, preeclampsia is associated with unhealthy high levels of cholesterol which increase the risk of heart complications for the mother. Even though the causes for this condition are unknown, there is evidence that maternal blood vessels do not work properly, which is associated with high levels of inflammation and leads to high blood pressure. However, how this malfunction of the blood vessels develops is not known. Therefore, our lab has been studying the mechanisms for the disturbed blood vessel function as we look for new strategies for treatment to improve maternal and newborn health outcomes. Recently, we have been focusing on a new potential mechanism that brings together two proteins (LOX-1 and AT1) that are each associated with 'bad' LDL cholesterol (which is highly present in women with preeclampsia). These proteins are known to increase inflammation and damage blood vessel function, and may therefore cause vascular disease. For our studies, we will use a mouse model of preeclampsia to evaluate blood vessel function and we will determine whether this is due to the combined action of the proteins described above. We will also use cells from the umbilical cord of normal and preeclamptic pregnancies to assess whether these proteins are working together and how they could impact not only maternal, but also fetal health. Our research goal is to study the mechanisms affecting blood vessel function during preeclampsia in order to develop future therapeutic strategies to improve maternal and newborn health.