Specialized vascular beds exist in various organs and often reflected their unique functions. For example, sinusoids are specialized, fenestrated blood vessels found in the bone marrow and liver, which also happen to be sites of hematopoiesis during embryogenesis. The placenta has two sets of unique, embryonic-derived vessels that participate in maternal-fetal nutrient exchange: the fetal capillary plexus that carries fetal blood and trophoblast vessels that carry maternal blood. Proper formation of these vascular channels in the embryo and placenta are essential for fetal organ growth, development, and function, and disrupting the signaling pathways underlying vascular development can result in embryonic defects and fetal demise. Decades of work have highlighted the importance of various molecules in vascular development. For example, vascular endothelial growth factor (VEGF) ligands transduce growth signals through VEGF receptors (VEGFR) to promote endothelial migration, proliferation, and survival, while vascular endothelial (VE-)cadherin, an endothelial cell-cell adhesion protein, controls vascular integrity, permeability, and signaling. The majority of these studies have focused on blood and lymphatic vessel development, and relatively little is known about the role of these pathways in regulating growth of sinusoidal vessels and placental vessels. This thesis is comprised of three studies that investigate the roles of the ligand VEGF-C, its main receptor VEGFR3, and their effector VE-cadherin in sinusoidal, lymphatic, and placental vascular development. In the first study, we demonstrate that VEGF-C/VEGFR3 and VE-cadherin exhibit reciprocal regulation to govern sinusoidal and lymphatic growth. Loss of VEGF-C/VEGFR3 or gain of VE-cadherin disrupts sinusoidal and lymphatic vessel growth, resulting in hematopoietic defects and lymphedema. In the second study, we show that VEGF-C signaling is also important for the formation of the fetal capillary plexus in the placenta. We demonstrate that in the absence of fetal-derived VEGF-C, maternal VEGF-C can compensate and support fetal capillary growth. In our third and final study, we investigate the role of VE-cadherin in trophoblasts during their invasion and connection to maternal blood vessels to bring maternal blood into the placenta. We find that deletion of VE-cadherin from trophoblasts compromises their ability to invade and replace maternal blood vessels, resulting in reduced maternal blood in the placenta and a preeclamptic-like phenotype. Altogether, these studies uncover novel regulators of vascular growth that enable organ-specific functions and identify opportunities for regeneration of sinusoidal, lymphatic, and placental vessels and therapeutic interventions for preeclampsia. These studies additionally open up new areas for future investigation, particularly in the field of placenta biology with the development of new genetic tools.