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PubMed2005

Factor XIII Val34Leu polymorphism and gamma-chain cross-linking at the site of microvascular injury in healthy and coumadin-treated subjects.

Fibrin (Fn) cross-linking by activated factor (F) XIII is essential for clot stability. In vitro, a common Leu34 polymorphism of the FXIIIA-subunit increases the rate of thrombin-mediated FXIII activation, but not cross-linking activity upon complete FXIII activation. The effect of FXIII Val34Leu polymorphism on fibrin(ogen) cross-linking in vivo when vascular injury triggers the blood coagulation has not been studied yet. Using quantitative immunoblotting with antibodies raised against FXIIIA-subunits, fibrinogen, and gamma-gamma-dimers, the rates of FXIIIA cleavage and fibrin(ogen) cross-link formation in the fluid phase of 30-s blood samples collected at the site of microvascular injury were compared in the Leu34-positive and -negative healthy individuals and patients on long-term oral anticoagulation. In addition to accelerated FXIII activation, in healthy subjects the presence of FXIII Leu34 allele was associated with increased soluble gamma-gamma-dimer formation by 40% (1355 +/- 17 microg L(-1) for Leu34 carriers vs. 804.3 +/- 17 microg L(-1) for Leu34 non-carriers; P = 0.028) at the site of microvascular injury. This solution phase effect was abolished in coumadin-treated patients (369.4 +/- 75.9 microg L(-1) for Leu34 carriers vs. 290.5 +/- 35.9 microg L(-1) for Leu34 non-carriers; P > 0.05). The present study indicates that the Leu34 allele affects soluble gamma-gamma-dimer formation in untreated individuals, but not in those receiving acenocoumarol. Our data may help elucidate the impact of the FXIII Val34Leu polymorphism on Fn cross-linking in vivo and its modulation by oral anticoagulants.

Adult↗
PubMed1987

Coagulation factor XIII A and B subunits in bone marrow and liver transplantation.

The polymorphism of the coagulation factor XIIIA and B subunits was determined before and after bone marrow or liver transplantation. It could be shown that the FXIIIA phenotype of the recipient was replaced by donor phenotype after bone marrow transplantation, whereas the phenotype of FXIIIB remained of recipient origin. In contrast, the FXIIIB phenotype changed to donor type after orthotopic liver transplantation but not the FXIIIA phenotype. The results indicate that the FXIIIA protein is produced in hemopoiesis, most likely in megakaryocytes and FXIIIB protein in the liver. Depending on the site of synthesis, FXIII alleles can be used as a marker in engraftment of FXIIIA-incompatible bone marrow transplantation or as a marker in FXIIIB-incompatible orthotopic liver transplantation.

Alleles↗