ABSTRACT
Following the initial stages of blastocyst implantation and decidualization, formation of the placenta begins in earnest. During this process cells from the trophectoderm, the outer layer of the blastocyst, must proliferate and differentiate into the chorionic villus tree that forms the placenta proper. The human placenta, which is classified as hemochorial, differs from commonly studied animal models such as mice, rats, and rabbits in that it is highly invasive – hemiallogeneic fetal cytotrophoblasts (CTBs) invade uterine tissues, where they reside in an apparently symbiotic fashion for the entirety of gestation. In mammalian species the extent of decidualization correlates with the extent of trophoblast (TB) invasiveness.1,2 In this regard, the human endometrium, which shows the greatest transformation during pregnancy, plays a critical role by expressing molecules that directly or indirectly govern formation of the placenta. Undoubtedly the converse is true as we also know that invading CTBs induce decidualization and the unique process whereby the maternal vasculature is remodeled into a high-flow system that delivers blood to the placenta. In this chapter, we examine the current state of understanding regarding factors that regulate CTB differentiation and invasion during formation of the human placenta with a particular focus on the maternal-fetal interface (decidua basalis). We also consider aberrations in formation of the placenta and/or the maternal-fetal interface that lead to pregnancy complications of which preeclampsia (PE) is a prime example.
