In pregnancies complicated by severe fetal growth restriction secondary to placental insufficiency, the only option that obstetricians have is to proceed with delivery, oftentimes quite prematurely, in order to avert stillbirth. Existing clinical data, however, suggests that timing of delivery and existing ultrasound parameters do not substantially affect survival or long-term outcome. Thus, understanding the mechanisms underlying placental insufficiency and fetal growth restriction are needed if we are to be able to actually improve outcomes. Clinical data also demonstrate that fetuses/placentas that demonstrate abnormal blood flow, (e.g. abnormal umbilical artery Doppler waveforms), are the ones that suffer the worst outcomes. Morphometric studies have shown that these placentas do not form a proper vascular tree, and much of the defective angiogenesis is purported to occur in later pregnancy. Thus, the goal of this project is to determine mechanisms underlying impaired fetoplacental angiogenesis in human fetoplacental endothelial cell models.