Embryo in uterine implantation is a complex and rnultifactor-related process and is a downstream and ideal point for woman fertility control. Understanding the cellular and molecular mechanism of implantation is a prerequisite for development of anti-implantation contraceptives. In spite of considerable accumulation of information from the laboratory animals that has been achieved, it is difficult to generate such information in human due to ethical restriction and x-perimental limitation, and the present knowledge for understanding the definitive mechanisms which control these events remains elusive. Embryo implantation can also occur outside uterus. Some women with abdominal pregnancies could successfully complete the processes of gesta-tion nd bear normal babies, implying that implantation itself may be not an endo-metrium-specific process. Reproductive biologists should cooperate with gynecologists to further comparatively study the molecular and cellular mechanisms of implantation normally occurring in endometrium and abnormally appearing outside uterine cavity. Such collaborative studies may generate new important information for developing anti-implantation contraceptive and for tech-niques of accu- rate diagnosis of ectopic pregnancy. A specially designed GnRH-2 analog and a combination use of low dose RU486 and gossypol as anti-implantation contraceptives have been suggested.
The target molecule of monoclonal antibody AA98 (AA for short) is a new vascular endothelial cell related factor and plays a role in angiogenesis as indicated by the previous data. To investigate its role in angiogenesis and placentation in primate, we examined its expression in the implantation sites on D17, 19, 28 and 34 of gestation in rhesus monkey by immunohistochemistry and Western immunoblot. Western blot analysis showed that the primary antibody used in this study was specific for its epitope. AA protein was mainly expressed in small blood vessels and in some cytotrophoblast cells. The AA staining was found mainly in the endothelial cells and vascular small muscle.This observation supported the AA's role in angiogenesis. AA was spatio-temporarily expressed in cytotrophoblasts: weak in proliferating trophoblast within cell column and endovascular trophoblast, strong in trophoblastic subpopulation within the basal plate and vascular trophoblast; AA staining within the basal plate was down-regulated during early placentation. The shift of AA98 expression in extravillous trophoblasts suggestes a role of this new factor during the course of cytotrophoblast metastasis and spiral artery remodeling. The spatio-temporarily expression indicats that AA98 could be also used as a trophoblast cellular marker to characterize the acquisition of a vascular endothelial and invasive phenotype.
