Maternal platelets at the first trimester maternal-placental interface – Small players with great impact on placenta development

In human pregnancy, maternal platelet counts decrease with each trimester, reaching a reduction by approximately ten percent at term in uncomplicated cases and recover to the levels of the non-pregnant state a few weeks postpartum. The time when maternal platelets start to occur in the early human placenta most likely coincides with the appearance of loosely cohesive endovascular trophoblast plugs showing capillary-sized channels by mid first trimester. At that time, platelets accumulate in intercellular gaps of anchoring parts of trophoblast columns and start to adhere to the surface of placental villi and the chorionic plate. This is considered as normal process that contributes to placenta development by acting on both the extravillous- and the villous trophoblast compartment. Release of platelet cargo into intercellular gaps of anchoring cell columns may affect partial epithelial-to-mesenchymal transition and invasiveness of extravillous trophoblasts as well as deposition of fibrinoid in the basal plate. Activation of maternal platelets on the villous surface leads to perivillous fibrin-type fibrinoid deposition, contributing to the shaping of the developing placental villi and the intervillous space. In contrast, excess platelet activation at the villous surface leads to deregulation of the endocrine activity, sterile inflammation and local apoptosis of the syncytiotrophoblast. Platelets and their released cargo are adapted to pregnancy, and may be altered in high-risk pregnancies. Identification of different maternal platelet subpopulations, which show differential procoagulant ability and different response to anti-platelet therapy, are promising new future directions in deciphering the role of maternal platelets in human placenta physiology.