Does the Defective Plasma Coagulation Cascade Also Account for Embryonic Bleeding?
Insights into this question have come from analysis of mouse models with defective blood clotting caused by factors downstream of thrombin activation. Mice without the transcription factor NF-E2 lack circulating platelets. 36 These mice die of hemorrhage, indicating that their clotting system is indeed defective. Surprisingly, embryonic development is not altered in these mice, and embryonic bleeding is also not reported. Consequently, insufficient platelet activation as a result of low thrombin levels would not necessarily explain embryonic bleeding in coagulation factor–deficient mice. Along the same lines, Suh and coworkers 37 reported that mice lacking the fibrinogen α-chain (which is required for effective thrombus formation) do not suffer from disturbances in embryonic development or from embryonic bleeding. Thus, both downstream events of thrombin activation, platelet activation and fibrinogen cleavage, do not seem to be important in controlling embryonic blood loss.
