Platelet factor XIII-A regulates platelet function and promotes clot retraction and stability

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art_MITCHELL_Platelet_factor_XIIIA_regulates_platelet_function_and_promotes_2023.PDF (5 MB)
Citações na Scopus
3
Tipo de produção
article
Data de publicação
2023
DOI
Scopus
Web of Science
PubMed
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Título do Volume
Editora
ELSEVIER
Autores
MITCHELL, Joanne L.
LITTLE, Gemma
BYE, Alexander P.
UNSWORTH, Amanda J.
KRIEK, Neline
SAGE, Tanya
STAINER, Alexander
SANGOWAWA, Ibidayo
MORROW, Gael B.
Citação
RESEARCH AND PRACTICE IN THROMBOSIS AND HAEMOSTASIS, v.7, n.5, article ID e100200, 15p, 2023
Projetos de Pesquisa
Unidades Organizacionais
Fascículo
Resumo
Background: Factor XIII (FXIII) is an important proenzyme in the hemostatic system. The plasma-derived enzyme activated FXIII cross-links fibrin fibers within thrombi to increase their mechanical strength and cross-links fibrin to fibrinolytic inhibitors, specifically & alpha;2-antiplasmin, to increase resistance to fibrinolysis. We have previously shown that cellular FXIII (factor XIII-A [FXIII-A]), which is abundant in the platelet cytoplasm, is externalized onto the activated membrane and cross-links extracellular substrates. The contribution of cellular FXIII-A to platelet activation and platelet function has not been extensively studied.Objectives: This study aims to identify the role of platelet FXIII-A in platelet function. Methods: We used normal healthy platelets with a cell permeable FXIII inhibitor and platelets from FXIII-deficient patients as a FXIII-free platelet model in a range of platelet function and clotting tests.Results: Our data demonstrate that platelet FXIII-A enhances fibrinogen binding to the platelet surface upon agonist stimulation and improves the binding of platelets to fibrinogen and aggregation under flow in a whole-blood thrombus formation assay. In the absence of FXIII-A, platelets show reduced sensitivity to agonist stimulation, including decreased P-selectin exposure and fibrinogen binding. We show that FXIII-A is involved in platelet spreading where a lack of FXIII-A reduces the ability of platelets to fully spread on fibrinogen and collagen. Our data demonstrate that platelet FXIII-A is important for clot retraction where clots formed in its absence retracted to a lesser extent.Conclusion: Overall, this study shows that platelet FXIII-A functions during thrombus formation by aiding platelet activation and thrombus retraction in addition to its antifibrinolytic roles.
Palavras-chave
clot retraction, factor XIII, fibrinogen, fibrinolysis, platelet activation, platelet
URI
https://observatorio.fm.usp.br/handle/OPI/56210
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Coleções
Artigos e Materiais de Revistas Científicas - FM/Outros
Artigos e Materiais de Revistas Científicas - LIM/64