Control of human trophoblast function

Trophoblast is an embryonic tissue which exerts a crucial role during implantation and placentation. Both processes can only take place through a significant change in the uterine wall in response to different modulatory molecules, among which steroid and peptide hormones, as well as local factors including prostanoids. This transformation, aimed at creating a favourable environment for receiving the blastocyst, and permitting embryo-fetal development, is represented by a complex series of events termed decidualization. Implantation consists of the blastocyst penetrating the luminal epithelium, crossing the basal lamina and, finally, embedding itself in the stroma. During implantation a syncytiotrophoblast (ST) is formed, which begins to invade the maternal tissue. Afterwards, vascularization of the trophoblast occurs in order to establish and maintain a feto-placental vasculature. Simultaneously, maternal vascular remodeling takes place so as to generate a utero-placental circulation. For successful placentation to occur, a highly orchestrated control of vasculogenesis, angiogenesis, and trophoblast functions is required. This is operated by a large number of heterogeneous factors which act by both autocrine and paracrine mechanisms.Here we review the control of trophoblast function, highlighting the aspects which may improve management of pregnancy complications.In order for implantation to occur, endometrium has to be changed into decidua. This process consists in modifying endometrial stromal cells, uterine glands and vessels, as well as the population of uterine immune cells. In humans, unlike other species [1], decidualization is independent of the blastocyst's presence in the uterine cavity and begins in the late secretory phase of the menstrual cycle. It is evoked by progesterone, as well as by regulatory agents able to enhance cyclic AMP (cAMP) levels [2,3]. Decidualization continues in pregnancy, and it is thought to regulate subsequent trophoblast invasio