Placental angiogenesis requires proliferation, migration, and differentiation of endothelial cells [1]. This process involves the formation of the placental microvasculature and macrovasculature and is a physiological process that must be finely regulated. There are large numbers of caveolae in the plasma membrane of endothelial cells [2]. Caveolae are lipid domains that have Caveolin-1 (Cav-1) as their marker protein. Cav-1 can bind different proteins and thus promote interactions between receptors, channels, and signaling proteins [3]. Our main objective was to evaluate the role of the caveolae in the formation of the placental vasculature. Placental microvascular endothelial cells (hPMEC) and the EA.hy926 cell line (ATCC®CRL-2922™) were used. Cav-1 gene and protein expression, and localization were evaluated. Cells were treated with 5mM methyl-β-cyclodextrin (MβCD) to disrupt caveolae [4]. Cell viability was assessed by MTT and cell migration by wound healing assay. Cav-1 was located in the plasma membrane of placental endothelial cells. MβCD significantly reduced cell migration in EA.hy926 cells (n=4; p<0.05) and in hPMEC cells (n=4; p<0.0001). Our results suggest that an intact caveolar structure is necessary for the proper migration of placental endothelial cells. Any disturbance could cause aberrant angiogenesis leading to serious pregnancy disorders.