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- W4247804970 abstract "This chapter focuses on the unique process by which the human placenta normally forms, and how changes can lead to serious pregnancy complications such as preeclampsia. Special emphasis is placed on work from the principal author's laboratory that led to the discovery that the subset of placental cells, termed cytotrophoblasts, that invade the uterus and form vascular connections with the resident maternal vessels undergo a novel transformation from an epithelial cell of ectodermal origin to a vascular-like cell with a myriad of endothelial-like properties. The human placenta's unique anatomy is due in large part to differentiation of its ectodermally derived progenitors, termed cytotrophoblasts. In floating villi, cytotrophoblasts differentiate by fusing to form multinucleate syncytiotrophoblasts whose primary function—transport—is ideally suited to their location at the villus surface. In anchoring villi, cytotrophoblasts also fuse, but many remain as single cells that detach from their basement membrane and aggregate to form cell columns. Cytotrophoblasts at the distal ends of these columns attach to, and then deeply invade the uterus and its arterioles. As a result of endovascular invasion, the cells replace the endothelial and muscular linings of uterine arterioles, a process that initiates maternal blood flow to the placenta and greatly enlarges the vessel diameter. Paradoxically, the cells invade only the superficial portions of uterine venules. Preeclampsia and hypertensive diseases of pregnancy are leading causes of maternal death. Anatomic examination shows that the area of the placenta most affected by this syndrome is the fetal–maternal interface. Cytotrophoblast invasion of the uterus is shallow, and endovascular invasion does not proceed beyond the terminal portions of the spiral arterioles." @default.
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- W4247804970 date "1990-01-01" @default.
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- W4247804970 title "Editorial" @default.
- W4247804970 doi "https://doi.org/10.1016/s0143-4004(05)80436-9" @default.
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