Evidence for the production of platelet-activating factor by murine embryos and its putative role in the maternal physiology.

Thrombocytopenia has been shown to be an initial maternal response to conception. We investigated a potent bioactive lipid, platelet-activating factor (PAF), as one of the candidates derived from embryos to induce the decrease of platelet counts in maternal blood. First, we examined the potential of murine embryos to liberate PAF. In brief, twenty to thirty murine two-cell embryos of C57BL/6 mice were cultured in Whitten's medium for 24 h. The supernatant of the medium was collected and the total was extracted. After developing the lipid on thin-layer chromatography, the area corresponding to authentic PAF was scraped off and the lipid was extracted. The embryo-derived PAF was quantified by platelet aggregation using rabbit whole blood, and the presence of PAF was further confirmed by the addition of a PAF-receptor antagonist, SRI63-441. The results showed that a significant amount of PAF (ca. 10 ng/ml) was recovered from the lipid extract, whereas little platelet-aggregating activity was observed in the presence of SRI63-441. Second, the physiological function of murine platelets was examined using authentic PAF. When PAF (up to 83 micrograms/ml) was added to the murine platelets suspended in the whole blood, it neither induced platelet aggregation nor reduced the number of platelets. Considering these results, it is considered that PAF released from the embryos does not directly act on maternal platelets, but transduces its signal to the maternal host via some other bioactive substance.