CT functions as a stem cell and is located on the villous surface. CT expresses epidermal growth factor receptor (EGF-R), which binds with EGF secreted by the decidua (3). It has been postulated that through a paracrine-like mechanism, EGF-R and its ligand may provide growth stimulation for CT (4). CT differentiates along two main pathways. On the villous surface, CT fuses to form the overlying ST. This process results in expansion of the surface area of chorionic villi in the developing placenta. In the second pathway, CT in the trophoblastic column differentiates into villous IT and then into implantation site IT in the placental site or chorionic-type IT in the chorion laeve (5). The mechanisms underlying the differentiation of CT are unclear. Recently, however, expression of syncytin has been shown to be involved in the fusion of CT into ST (6) and downregulation of Id-2 is associated with differentiation into implantation site IT (7). In addition, it has been shown that CT expresses the aN isoforms of p63, whereas chorionic-type IT in the fetal membranes expresses the TA isoforms (8). Implantation site IT and ST do not express either of the p63 isoforms. As p63 isoforms have specific functions including those that relate to regulation of apoptosis and proliferation, these findings suggest that p63 may act as a molecular switch. Thus, turning off or turning on specific p63 isoforms may in turn control trophoblastic differentiation and placental development. The expression of the aN isoform in CT is consistent with its proposed function of maintaining basal or stem cells in a state where they are capable of proliferation and differentiation, perhaps by preventing cell-cycle arrest and inhibiting apoptosis (9). Thus, as CT differentiates into either ST or implantation site IT in the trophoblastic columns, there is a dramatic decrease in aNp63 expression, which may contribute to cell-cycle arrest (10) as evidenced by the virtual absence of Ki-67 labeling in ST and implantation site IT (5,11).

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