RGD Reference Report - Factor XIII A subunit-deficient mice developed severe uterine bleeding events and subsequent spontaneous miscarriages. - Rat Genome Database

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

Authors: Koseki-Kuno, S  Yamakawa, M  Dickneite, G  Ichinose, A 
Citation: Koseki-Kuno S, etal., Blood. 2003 Dec 15;102(13):4410-2. Epub 2003 Aug 21.
RGD ID: 10450744
Pubmed: PMID:12933578   (View Abstract at PubMed)
DOI: DOI:10.1182/blood-2003-05-1467   (Journal Full-text)

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.

RGD Manual Disease Annotations    Click to see Annotation Detail View

Objects Annotated

Genes (Rattus norvegicus)
F13a1  (coagulation factor XIII A1 chain)

Genes (Mus musculus)
F13a1  (coagulation factor XIII, A1 subunit)

Genes (Homo sapiens)
F13A1  (coagulation factor XIII A chain)


Additional Information