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From the W. M. Keck Center for Transgene Research and theDepartment of Chemistry and Biochemistry, University of NotreDame, Notre Dame, Indiana
In humans, maternal fibrinogen (Fg) is required to support
pregnancies by maintaining hemostatic balance and stabilizing
uteroplacental attachment at the fibrinoid layer found at the
fetal-maternal junction. To examine relationships between low Fg levels
and early fetal loss, a genetic model of afibrinogenemia was
developed. Pregnant mice homozygous for a deletion of the Fg-
chain, which results in a total Fg deficiency state
(FG-/-), aborted the fetuses
at the equivalent gestational stage seen in humans. Results obtained
from timed matings of FG-/- mice
showed that vaginal bleeding was initiated as early as embryonic day
(E)6 to 7, a critical stage for maternal-fetal vascular
development. The condition of afibrinogenemia retarded embryo-placental
development, and consistently led to abortion and maternal
death at E9.75. Lack of Fg did not alter the extent or distribution
pattern of other putative factors of embryo-placental
attachment, including laminin, fibronectin, and
Factor XIII, indicating that the presence of
fibrin(ogen) is required to confer sufficient stability at
the placental-decidual interface. The results of these studies
demonstrate that maternal Fg plays a critical role in maintenance of
pregnancy in mice, both by supporting proper
development of fetal-maternal vascular communication and
stabilization of embryo implantation.
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