Vascular development occurs through the processes of angiogenesis and vasculogenesis (1,2). Angiogenesis is the process of neovascularization from pre-existing blood vessels, whereas vasculogenesis is the process of blood vessel generation from angioblast precursor cells. The human placenta undergoes high levels of both angiogenesis and vasculogenesis during fetal development (3). Additionally, the placenta undergoes a process of vascular mimicry (also referred to as pseudovasculogenesis), in which the placental cytotrophoblasts convert from an epithelial to an endothelial phenotype during normal placental development (4). When placental vascular development is deranged, serious complications such as intrauterine growth restriction (IUGR) and preeclampsia can occur. This chapter discusses placental vascular development during health and in disease, with an emphasis on the role of placental angiogenic factors in these processes.
PLACENTAL VASCULAR DEVELOPMENT IN HEALTH
Placentation, which is characteristic of and specific to mammals, allows for the development of the fetus within a protective maternal environment (5). The placenta provides oxygen (O2) and nutrients to, and transfers wastes from, the developing fetus. The placenta is a highly vascular organ, containing both embryonic and maternal blood vessels (Figure 161.1; for color reproduction, see Color Plate 161.1).
During embryonic development, the blastocyst separates into two cell populations: an outer polarized cell layer (the trophoectoderm) and the nonpolarized inner cell mass. The trophoectoderm gives rise to extraembryonic trophoblasts, whereas the inner cell mass is destined to form the embryo proper.
Implantation of the blastocyst into the uterine wall, which occurs approximately 1 week after fertilization, involves a complex interplay between the trophoblasts and maternal cells.