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Publication : Factor XIII A subunit-deficient mice developed severe uterine bleeding events and subsequent spontaneous miscarriages.

First Author  Koseki-Kuno S Year  2003
Journal  Blood Volume  102
Issue  13 Pages  4410-2
PubMed ID  12933578 Mgi Jnum  J:86919
Mgi Id  MGI:2682463 Doi  10.1182/blood-2003-05-1467
Citation  Koseki-Kuno S, et al. (2003) Factor XIII A subunit-deficient mice developed severe uterine bleeding events and subsequent spontaneous miscarriages. Blood 102(13):4410-2
abstractText  To understand the molecular pathology of factor XIII (FXIII) deficiency in vivo, its A subunit (FXIIIA)-knockout (KO) mice were functionally analyzed. Although homozygous FXIIIA female KO mice were capable of becoming pregnant, most of them died due to excessive vaginal bleeding during gestation. Abdominal incisions revealed that the uteri of the dead mice were filled with blood and that some embryos were much smaller than others within a single uterus. A series of histologic examinations of the pregnant animals suggested that massive placental hemorrhage and subsequent necrosis developed in the uteri of the FXIIIA KO mice on day 10 of gestation. This was true regardless of the genotypes of fetuses. These results are reminiscent of spontaneous miscarriage in pregnant humans with FXIII deficiency and indicate that maternal FXIII plays a critical role in uterine hemostasis and maintenance of the placenta during gestation.
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