Factor XIII deficiency does not prevent FeCl
factor XIII
ferric chloride
fibrinogen
platelets
thrombosis
transglutaminase
Journal
Research and practice in thrombosis and haemostasis
ISSN: 2475-0379
Titre abrégé: Res Pract Thromb Haemost
Pays: United States
ID NLM: 101703775
Informations de publication
Date de publication:
Jan 2020
Jan 2020
Historique:
received:
10
09
2019
revised:
04
10
2019
accepted:
13
10
2019
entrez:
29
1
2020
pubmed:
29
1
2020
medline:
29
1
2020
Statut:
epublish
Résumé
The compositions of venous (red blood cell-rich) and arterial (platelet-rich) thrombi are mediated by distinct pathophysiologic processes; however, fibrin is a major structural component of both. The transglutaminase factor XIII (FXIII) stabilizes fibrin against mechanical and biochemical disruption and promotes red blood cell retention in contracted venous thrombi. Previous studies have shown factor XIII (FXIII) inhibition decreases whole blood clot mass and therefore, may be a therapeutic target for reducing venous thrombosis. The role of FXIII in arterial thrombogenesis is less studied, and the particular contribution of platelet FXIII remains unresolved. To determine whether FXIII reduction prevents experimental arterial thrombogenesis. Using wild-type mice and mice with genetically imposed deficiency in FXIII, we measured thrombus formation and stability following ferric chloride-induced arterial thrombosis. We also determined the impact of FXIII on the mass of contracted platelet-rich plasma clots. Following vessel injury, FXIII does not significantly alter the underlying pathophysiology of experimental arterial thrombus formation.
Sections du résumé
BACKGROUND
BACKGROUND
The compositions of venous (red blood cell-rich) and arterial (platelet-rich) thrombi are mediated by distinct pathophysiologic processes; however, fibrin is a major structural component of both. The transglutaminase factor XIII (FXIII) stabilizes fibrin against mechanical and biochemical disruption and promotes red blood cell retention in contracted venous thrombi. Previous studies have shown factor XIII (FXIII) inhibition decreases whole blood clot mass and therefore, may be a therapeutic target for reducing venous thrombosis. The role of FXIII in arterial thrombogenesis is less studied, and the particular contribution of platelet FXIII remains unresolved.
OBJECTIVE
OBJECTIVE
To determine whether FXIII reduction prevents experimental arterial thrombogenesis.
METHODS
METHODS
Using wild-type mice and mice with genetically imposed deficiency in FXIII, we measured thrombus formation and stability following ferric chloride-induced arterial thrombosis. We also determined the impact of FXIII on the mass of contracted platelet-rich plasma clots.
RESULTS
RESULTS
Following vessel injury,
CONCLUSIONS
CONCLUSIONS
FXIII does not significantly alter the underlying pathophysiology of experimental arterial thrombus formation.
Identifiants
pubmed: 31989092
doi: 10.1002/rth2.12278
pii: S2475-0379(22)01952-5
pmc: PMC6971319
doi:
Types de publication
Journal Article
Langues
eng
Pagination
111-116Informations de copyright
© 2019 The Authors. Research and Practice in Thrombosis and Haemostasis published by Wiley Periodicals, Inc on behalf of International Society on Thrombosis and Haemostasis.
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