Is Syndecan-1 the mediator of the fine regulation of embryonic invasion depth by means of apoptosis and the related decision on regular or pathological implantation in humans and mice?

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Within the project represented the embryonic implantation into the maternal endometrium as an interface on the course of pregnancy is supposed to be examined . The invasion depth of the conceptus into the maternal endometrial stroma is of paramount importance. Too low invasion in the sense of "shallow implantation" can lead to life-threatening diseases of mother and child during pregnancy. Equally dangerous is an excessive invasion, which can cause placenta detachment problems possibly leading to life-threatening situations during and after child birth. That the control of implantation is often not carried out correctly describes a study showing that in fact 60% of conceptions in the early and mostly undiscovered pre-clinical stages of pregnancy do not develop correctly. Since the operation of an adequate placentation and implantation are not fully understood so far, the cellular mechanisms underlying the regulation of the exact depth of invasion shall be investigated herein. Therefore, the question of how the space needed for a proper implantation of the embryo in the maternal tissue is created and how the correct regulation of invasion depth is orchestered is supposed to be answered . The chemokine receptor Syndecan-1 appears to play a role in the course of embryonic implantation, especially in the mediation of apoptosis. Herein it will be clarified which signaling pathways Syndecan-1 utilizes to induce apoptosis and how it regulates therewith the invasion depth of the conceptus to facilitate a proper implantation. Furthermore, it should be investigated, whether a dysregulated Syndecan-1 expression may provoke the onset of pregnancy disorders and metabolic changes of the embryos. The role of autophagy and hypoxia and their influence on apoptosis and thus regulation of embryonic invasion depth should also be further identified.