Literature DB >> 15350843

Factor XIII Val34Leu polymorphism modulates the prothrombotic and inflammatory state associated with atrial fibrillation.

Francisco Marín1, Javier Corral, Vanessa Roldán, Rocío González-Conejero, María Luz del Rey, Francisco Sogorb, Gregory Y H Lip, Vicente Vicente.   

Abstract

UNLABELLED: Atrial fibrillation (AF) has been shown to confer a prothrombotic or hypercoagulable state, which could be related to inflammation. Factor XIII (FXIII) catalyses the cross-linking of fibrin monomers, increasing clot resistance; specifically, a common polymorphism, Val34Leu, in the FXIII-A subunit gene has been associated with more rapid FXIII activation. We hypothesised a role for this polymorphism in the prothrombotic state and inflammation in AF, and tested this hypothesis by measurement of indices of coagulation (tissue factor (TF) and fibrinogen), inflammation (interleukin-6 (IL6)) and platelet activation (soluble P selectin (sPsel)).
METHODS: We studied 90 stable outpatients (73 +/- 8 years) with persistent AF. The FXIII Val34Leu polymorphism was determined by polymerase chain reaction-allelic specific restriction assay (PCR-ASRA). Prevalence of Val34Leu polymorphism of patients was compared to 585 unrelated subjects from the same geographical area. Plasma fibrinogen (Clauss), TF, IL6 and sPsel (all ELISA) were quantified in patient group. Research indices were compared to 74 controls in sinus rhythm with similar clinical characteristics.
RESULTS: There were no statistical differences in FXIII polymorphism prevalence between AF patients and controls. Patients carrying the Leu34 allele had higher plasma levels of TF, IL6 and sPsel (all P < 0.05) compared to controls. Plasma IL6 and TF levels were significantly correlated (Spearman coefficient, r = 0.33, P < 0.01). On multivariate analysis, the Leu34 allele was independently associated with IL6 levels (P < 0.01), whereas TF levels were only associated with IL6 concentrations. However, sPsel and fibrinogen levels were not related to Leu34 allele.
CONCLUSION: FXIII Val34Leu polymorphism was independently associated with IL6 levels in AF. The Leu34 allele may potentially influence the prothrombotic state in these patients by modulating the inflammatory state.

Entities:  

Mesh:

Substances:

Year:  2004        PMID: 15350843     DOI: 10.1016/j.yjmcc.2004.06.001

Source DB:  PubMed          Journal:  J Mol Cell Cardiol        ISSN: 0022-2828            Impact factor:   5.000


  5 in total

1.  Joint detection of association, imprinting and maternal effects using all children and their parents.

Authors:  Miao Han; Yue-Qing Hu; Shili Lin
Journal:  Eur J Hum Genet       Date:  2013-03-27       Impact factor: 4.246

2.  Transglutaminase factor XIII promotes arthritis through mechanisms linked to inflammation and bone erosion.

Authors:  Harini Raghu; Carolina Cruz; Cheryl L Rewerts; Malinda D Frederick; Sherry Thornton; Eric S Mullins; Jonathan G Schoenecker; Jay L Degen; Matthew J Flick
Journal:  Blood       Date:  2014-10-21       Impact factor: 22.113

3.  FXIII-A Leu34 genetic variant in premature coronary artery disease: a genotype--phenotype case control study.

Authors:  Johanne Silvain; Ana Pena; Jean-Baptiste Vignalou; Jean-Sébastien Hulot; Sophie Galier; Guillaume Cayla; Anne Bellemain-Appaix; Olivier Barthélémy; Farzin Beygui; Claire Bal-dit-Sollier; Ludovic Drouet; John W Weisel; Gilles Montalescot; Jean-Phillippe Collet
Journal:  Thromb Haemost       Date:  2011-07-28       Impact factor: 5.249

4.  The inflammatory response is influenced by FXIII VAL 34 LEU polymorphism in a human LPS model.

Authors:  Florian M Kovar; Claudia L Marsik; Bernd Jilma; Christine Mannhalter; Christian Joukhadar; Oswald F Wagner; Georg Endler
Journal:  Wien Klin Wochenschr       Date:  2009       Impact factor: 1.704

5.  Inflammatory cytokines and atrial fibrillation: current and prospective views.

Authors:  Hadi Ar Hadi; Alawi A Alsheikh-Ali; Wael Al Mahmeed; Jassim M Al Suwaidi
Journal:  J Inflamm Res       Date:  2010-08-30
  5 in total

北京卡尤迪生物科技股份有限公司 © 2022-2023.