Factor XIII deficiency does not prevent FeCl3‐induced carotid artery thrombus formation in mice

Abstract 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 bi...

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Autores principales:	Zhaoming Tang, Sravya Kattula, Lori A. Holle, Brian C. Cooley, Feng‐Chang Lin, Alisa S. Wolberg
Formato:	article
Lenguaje:	EN
Publicado:	Wiley 2020
Materias:	factor XIII ferric chloride fibrinogen platelets thrombosis transglutaminase Diseases of the blood and blood-forming organs RC633-647.5
Acceso en línea:	https://doaj.org/article/1f1037dc989d4d0f920178394e47c126
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spelling	oai:doaj.org-article:1f1037dc989d4d0f920178394e47c1262021-11-15T06:10:44ZFactor XIII deficiency does not prevent FeCl3‐induced carotid artery thrombus formation in mice2475-037910.1002/rth2.12278https://doaj.org/article/1f1037dc989d4d0f920178394e47c1262020-01-01T00:00:00Zhttps://doi.org/10.1002/rth2.12278https://doaj.org/toc/2475-0379Abstract 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 To determine whether FXIII reduction prevents experimental arterial thrombogenesis. 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 Following vessel injury, F13a+/+, F13a+/−, and F13a−/− mice developed occlusive arterial thrombi. FXIII deficiency did not significantly reduce the incidence or prolong the time to occlusion. FXIII deficiency also did not alter the timing of reflow events or decrease platelet‐rich clot mass. Conclusions FXIII does not significantly alter the underlying pathophysiology of experimental arterial thrombus formation.Zhaoming TangSravya KattulaLori A. HolleBrian C. CooleyFeng‐Chang LinAlisa S. WolbergWileyarticlefactor XIIIferric chloridefibrinogenplateletsthrombosistransglutaminaseDiseases of the blood and blood-forming organsRC633-647.5ENResearch and Practice in Thrombosis and Haemostasis, Vol 4, Iss 1, Pp 111-116 (2020)
institution	DOAJ
collection	DOAJ
language	EN
topic	factor XIII ferric chloride fibrinogen platelets thrombosis transglutaminase Diseases of the blood and blood-forming organs RC633-647.5
spellingShingle	factor XIII ferric chloride fibrinogen platelets thrombosis transglutaminase Diseases of the blood and blood-forming organs RC633-647.5 Zhaoming Tang Sravya Kattula Lori A. Holle Brian C. Cooley Feng‐Chang Lin Alisa S. Wolberg Factor XIII deficiency does not prevent FeCl3‐induced carotid artery thrombus formation in mice
description	Abstract 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 To determine whether FXIII reduction prevents experimental arterial thrombogenesis. 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 Following vessel injury, F13a+/+, F13a+/−, and F13a−/− mice developed occlusive arterial thrombi. FXIII deficiency did not significantly reduce the incidence or prolong the time to occlusion. FXIII deficiency also did not alter the timing of reflow events or decrease platelet‐rich clot mass. Conclusions FXIII does not significantly alter the underlying pathophysiology of experimental arterial thrombus formation.
format	article
author	Zhaoming Tang Sravya Kattula Lori A. Holle Brian C. Cooley Feng‐Chang Lin Alisa S. Wolberg
author_facet	Zhaoming Tang Sravya Kattula Lori A. Holle Brian C. Cooley Feng‐Chang Lin Alisa S. Wolberg
author_sort	Zhaoming Tang
title	Factor XIII deficiency does not prevent FeCl3‐induced carotid artery thrombus formation in mice
title_short	Factor XIII deficiency does not prevent FeCl3‐induced carotid artery thrombus formation in mice
title_full	Factor XIII deficiency does not prevent FeCl3‐induced carotid artery thrombus formation in mice
title_fullStr	Factor XIII deficiency does not prevent FeCl3‐induced carotid artery thrombus formation in mice
title_full_unstemmed	Factor XIII deficiency does not prevent FeCl3‐induced carotid artery thrombus formation in mice
title_sort	factor xiii deficiency does not prevent fecl3‐induced carotid artery thrombus formation in mice
publisher	Wiley
publishDate	2020
url	https://doaj.org/article/1f1037dc989d4d0f920178394e47c126
work_keys_str_mv	AT zhaomingtang factorxiiideficiencydoesnotpreventfecl3inducedcarotidarterythrombusformationinmice AT sravyakattula factorxiiideficiencydoesnotpreventfecl3inducedcarotidarterythrombusformationinmice AT loriaholle factorxiiideficiencydoesnotpreventfecl3inducedcarotidarterythrombusformationinmice AT brianccooley factorxiiideficiencydoesnotpreventfecl3inducedcarotidarterythrombusformationinmice AT fengchanglin factorxiiideficiencydoesnotpreventfecl3inducedcarotidarterythrombusformationinmice AT alisaswolberg factorxiiideficiencydoesnotpreventfecl3inducedcarotidarterythrombusformationinmice
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Factor XIII deficiency does not prevent FeCl3‐induced carotid artery thrombus formation in mice

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