Subscribe to RSS
DOI: 10.1055/s-0035-1570034
Implantation: Trophoblast-Endometrial Interactions
Publication History
Publication Date:
05 January 2016 (online)
The placenta is often referred to as the “after-birth” and its importance is highly overshadowed by the infant. Although several cultures pay homage to the critical role of the placenta, in most Western cultures it is simply discarded and incinerated. Yet the placenta is an amazing organ, formed from a fusion of mother and baby, which plays a critical role in the establishment and maintenance of pregnancy. The fetal placental cells, termed trophoblasts, are the first cells to differentiate in the developing embryos. These cells attach the embryo to the mother, invade the maternal endothelium, reform the maternal blood vessels, and ultimately establish the maternal–fetal interface. This interface is responsible for nutrient and gas exchange and establishing fetal immunity to the mother. The placenta is also a prolific endocrine organ capable of producing nearly every known hormone including several pregnancy-specific hormones.
We often think that studying the placenta is an area reserved for the maternal–fetal medicine specialists. It is clear that the placenta plays an important role in pregnancy-specific diseases. Epidemiological evidence suggests that these diseases, and others, are increased in pregnancies resulting from assisted reproductive technologies. Therefore, understanding the mechanisms responsible for trophoblast function, particularly in the first trimester, is important for the reproductive endocrinologist and biologist. It is unfortunate that very little is understood about the time between the transfer of embryo back to the uterus and the first pregnancy test. This issue of Seminars in Reproductive Medicine will discuss ways to study the developing trophoblast cells and many of the pitfalls associated with their study. In addition, we will review many in which the mother impacts trophoblast function and how the placenta, through epigenetic changes, sets the stage for fetal origins of adult disease.