Mechanistic studies of early pregnancy associated thrombocytopenia (EPAT) in the mouse.
The preimplantation period of uterine pregnancy is associated with the transient (first 4 days of gestation) expression of a state of early pregnancy-associated thrombocytopenia (EPAT), a phenomenon shown to be mediated by the embryo-derived EPAT factor, which presumably causes platelet activation and subsequent removal. We previously investigated the time course of production of EPAT factor in mouse embryo culture medium and found a correlation between the production of this factor and the in vivo platelet alterations in pregnant mice. The present paper supports the postulation that the EPAT factor and PAF-acether (a phospholipid platelet-activating factor) are related by providing data showing that PAF-acether may be responsible for the thrombocytopenia. Finally, data are presented to suggest that platelet activation, though not affecting the rate of ovulation, is important for successful ongoing pregnancy. Results suggest that the EPAT factor, produced by the fertilized egg, might act to signal uterine decidualization and/or modulate maternal immunological rejection of the implanting conceptus.
D000818:Animals; D001792:Blood Platelets / Q000502:physiology; D047108:Embryonic Development; D005260:Female; D051379:Mice; D010972:Platelet Activating Factor / Q000502:physiology; D010976:Platelet Count; D011247:Pregnancy / Q000097:blood; D011250:Pregnancy Complications, Hematologic / Q000097:blood / Q000209:etiology*; D013921:Thrombocytopenia / Q000097:blood / Q000150:complications* / Q000209:etiology
D010972:Platelet Activating Factor