دورية أكاديمية

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

التفاصيل البيبلوغرافية
العنوان: Platelet factor XIII-A regulates platelet function and promotes clot retraction and stability.
المؤلفون: Mitchell JL; Institute for Cardiovascular Research, University of Birmingham, Birmingham, UK., Little G; Institute for Cardiovascular and Metabolic Research, School of Biological Sciences, University of Reading, Reading, UK., Bye AP; School of Pharmacy, University of Reading, Reading, UK., Gaspar RS; Heart Institute, University of Sao Paulo School of Medicine, Sao Paulo, Brazil., Unsworth AJ; Department of Life Sciences, Faculty of Science and Engineering, Manchester Metropolitan University, Manchester, UK., Kriek N; Institute for Cardiovascular and Metabolic Research, School of Biological Sciences, University of Reading, Reading, UK., Sage T; Institute for Cardiovascular and Metabolic Research, School of Biological Sciences, University of Reading, Reading, UK., Stainer A; Institute for Cardiovascular and Metabolic Research, School of Biological Sciences, University of Reading, Reading, UK., Sangowawa I; Institute for Cardiovascular and Metabolic Research, School of Biological Sciences, University of Reading, Reading, UK., Morrow GB; Oxford University Hospitals NHS Foundation Trust, Blood Theme Oxford Biomedical Research Centre, Oxford, UK.; Radcliffe Department of Medicine, University of Oxford, Oxford, UK., Bastos RN; Oxford Nanoimaging, Oxford, UK., Shapiro S; Oxford University Hospitals NHS Foundation Trust, Blood Theme Oxford Biomedical Research Centre, Oxford, UK.; Radcliffe Department of Medicine, University of Oxford, Oxford, UK., Desborough MJR; Oxford University Hospitals NHS Foundation Trust, Blood Theme Oxford Biomedical Research Centre, Oxford, UK., Curry N; Oxford University Hospitals NHS Foundation Trust, Blood Theme Oxford Biomedical Research Centre, Oxford, UK.; Radcliffe Department of Medicine, University of Oxford, Oxford, UK., Gibbins JM; Institute for Cardiovascular and Metabolic Research, School of Biological Sciences, University of Reading, Reading, UK., Whyte CS; Aberdeen Cardiovascular & Diabetes Centre, School of Medicine, Medical Sciences and Nutrition, Institute of Medical Sciences, University of Aberdeen, Aberdeen, UK., Mutch NJ; Aberdeen Cardiovascular & Diabetes Centre, School of Medicine, Medical Sciences and Nutrition, Institute of Medical Sciences, University of Aberdeen, Aberdeen, UK., Jones CI; Institute for Cardiovascular and Metabolic Research, School of Biological Sciences, University of Reading, Reading, UK.
المصدر: Research and practice in thrombosis and haemostasis [Res Pract Thromb Haemost] 2023 Jun 07; Vol. 7 (5), pp. 100200. Date of Electronic Publication: 2023 Jun 07 (Print Publication: 2023).
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Elsevier Country of Publication: United States NLM ID: 101703775 Publication Model: eCollection Cited Medium: Internet ISSN: 2475-0379 (Electronic) Linking ISSN: 24750379 NLM ISO Abbreviation: Res Pract Thromb Haemost Subsets: PubMed not MEDLINE
أسماء مطبوعة: Publication: 2023- : [New York] : Elsevier
Original Publication: Hoboken, NJ : John Wiley & Sons, Inc., [2017]-
مستخلص: 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 α 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.
(© 2023 The Authors.)
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معلومات مُعتمدة: MR/T024054/1 United Kingdom MRC_ Medical Research Council
فهرسة مساهمة: Keywords: clot retraction; factor XIII; fibrinogen; fibrinolysis; platelet; platelet activation
تواريخ الأحداث: Date Created: 20230821 Latest Revision: 20240214
رمز التحديث: 20240214
مُعرف محوري في PubMed: PMC10439398
DOI: 10.1016/j.rpth.2023.100200
PMID: 37601014
قاعدة البيانات: MEDLINE
الوصف
تدمد:2475-0379
DOI:10.1016/j.rpth.2023.100200