Trophoblast invasion during implantation and placentation is critical for successful gestation and it is thought that invasion insufficiencies during placentation contribute to a number of obstetrical complications. However, relatively little is known regarding the regulation of this process and its link with the formation of new vascular beds during early pregnancy. Here, we review literature concerning the potential significance of inadequate uterine invasion as a contributor to the obstetrical complications of spontaneous abortion and preeclampsia. Studies have shown that both extrinsic and intrinsic factors involved in trophoblast invasion modulation seemed to be involved in some common obstetrical complications as early pregnancy loss and preeclampsia. Lipid molecules (i.e. prostaglandins, lysophosphatidic acid, anandamide), nitric oxide, metalloproteases and uterine natural killer cells, which are involved in implantation deficiencies, are also reported to be part of vascular abnormalities observed during preeclampsia. Trophoblast invasion together with placental vascularization reflects a complex interaction of regulatory factors. Understanding the regulation of trophoblast growth in the uterine matrix will provide much needed insight into implantation failure and placenta-related vascular insufficiencies.
Keywords: Preeclampsia, Trophoblast, intrinsic factors, pregnancy, placental vascularization
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