Implantation Site IT

The major function of implantation site IT is to establish the maternal-fetal circulation by invading the spiral arteries in the basal plate during early pregnancy (13). It has been suggested that the mechanisms underlying trophoblastic invasion are similar to those involved in tumor cell invasion (14,15). Because in both processes a variety of proteases, cell-adhesion molecules, growth factors and their receptors, and tumor-associated antigens including HLA-G and CD146 are expressed in both and there is also loss of E-cadherin expression (16). However, unlike malignant tumors, the invasion of implantation site IT is tightly regulated, confined spatially to the implantation site, and limited temporally to early pregnancy (4,13,17,18). Whereas, extensively infiltrating the endometrium of the basal plate, the implantation site IT invades only the inner third of the myometrium in the first trimester, decreasing to less than 10% of the myometrium by term. Although, the molecular mechanisms underlying the control of trophoblastic invasion are unclear, the invasive process can be modulated by both the trophoblast and the local microenvironment (4,17-19). Fusion of mononucleate implantation site intermediate trophoblastic cells with multinucleated cells leads to the loss of their invasive and migratory phenotype. Implantation site intermediate trophoblastic cells are not proliferative as they are negative for Ki-67, a proliferation marker, and are positive for several proteins, which are involved in the arrest of cell-cycle progression including p2lWAF1/CIP1 (20) and p57kip-2 (21). It is of interest that implantation site intermediate trophoblastic cells express cyclin E, but its biological significance is unknown at present (22).

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