Our lab focuses on the molecular mechanisms underlying the fetal sex-specific dysregulation of fetal endothelial function in complicated pregnancies, and the maternal obesity-associated fetal endothelial dysfunction and future health risks of the offspring. Our research utilizing multiple model systems including human placenta tissue, human cell models, and in vivo animal models.
Endothelial cells are a thin single layer of cells that lining the interior surface of blood vessels and lymphatic vessels. Dysregulation of endothelial cell function is associated with many cardiovascular and metabolic diseases. Children born to complicated pregnancies (such as preeclampsia and gestational diabetes) have increased risks of adult-onset cardiovascular disorders later in life, suggesting there are programming of fetal vascular/endothelial systems before birth. Maternal obesity is one of the prevalent risk factors that increases the overall risk of preeclampsia by 3-fold. Children born to obese mothers also exhibit higher blood pressure and increased risks of adverse cardiovascular outcomes in adulthood.
Our research aims to reveal the mechanisms controlling the complicated pregnancy-induced fetal sex-specific endothelial dysfunction in female and male fetal endothelial cells. Specifically, we are interested in 1) studying the sexual dimorphisms of complicated pregnancies-associated fetal endothelial dysfunction, 2) exploring the role of microRNAs in complicated pregnancies-induced fetal endothelial dysfunction, and 3) examining the effect of maternal obesity on fetal endothelial function and future cardiovascular risks of the offspring. Results from these studies would contribute to the identification of novel biomarkers or therapeutic targets for adult-onset cardiovascular disease in children born to complicated pregnancies.