Abstract
Development of the human placenta leads to two distinct trophoblast populations: the villous trophoblast primarily engaged in absorptive, exchange and endocrine functions, and the extravillous trophoblast (EVT) primarily engaged in remodeling the pregnant endometrium and its vasculature to achieve placental anchorage to the uterine wall and unhindered placental perfusion through low resistance uterine vessels. Both trophoblast populations arise by proliferation and differentiation of cytotrophoblast stem cells in the villus. Transforming growth factor (TGF)β, a homodimeric glycoprotein existing in several isoforms is a potent regulator of villous as well as extravillous trophoblast cell functions. This factor is produced by the placenta (primarily the syncytiotrophoblast), and more abundantly by the decidual cells. In the first trimester decidua, it is stored in the extracellular matrix, colocalized with a TGFβ binding and inactivating proteoglycan, decorin. The inactive decidual TGFβ can be activated by trophoblast derived proteases. TGFβ retards differentiation of the villous
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