دورية أكاديمية
أعرض في EDS

An extensional strain sensing mechanosome drives adhesion-independent platelet activation at supraphysiological hemodynamic gradients.

التفاصيل البيبلوغرافية
العنوان: An extensional strain sensing mechanosome drives adhesion-independent platelet activation at supraphysiological hemodynamic gradients.
المؤلفون: Zainal Abidin NA; The Australian Centre for Blood Diseases, Monash University, Melbourne, VIC, 3004, Australia., Poon EKW; Department of Medicine, St Vincent's Hospital, Melbourne Medical School, Faculty of Medicine, Dentistry & Health Sciences, The University of Melbourne, Fitzroy, VIC, 3065, Australia., Szydzik C; The Australian Centre for Blood Diseases, Monash University, Melbourne, VIC, 3004, Australia.; School of Engineering, RMIT University, La Trobe Street, Melbourne, VIC, 3004, Australia., Timofeeva M; Department of Mechanical Engineering, Faculty of Engineering and Information Technology, The University of Melbourne, Melbourne, VIC, 3010, Australia., Akbaridoust F; Department of Mechanical Engineering, Faculty of Engineering and Information Technology, The University of Melbourne, Melbourne, VIC, 3010, Australia., Brazilek RJ; The Australian Centre for Blood Diseases, Monash University, Melbourne, VIC, 3004, Australia., Tovar Lopez FJ; School of Engineering, RMIT University, La Trobe Street, Melbourne, VIC, 3004, Australia., Ma X; Medicinal Chemistry, Monash Institute of Pharmaceutical Sciences, Monash University, Parkville, VIC, 3052, Australia., Lav C; Department of Mechanical Engineering, Faculty of Engineering and Information Technology, The University of Melbourne, Melbourne, VIC, 3010, Australia.; CFD Methodology Group, Scuderia AlphaTauri F1, Bicester, OX26 4LD, UK., Marusic I; Department of Mechanical Engineering, Faculty of Engineering and Information Technology, The University of Melbourne, Melbourne, VIC, 3010, Australia., Thompson PE; Medicinal Chemistry, Monash Institute of Pharmaceutical Sciences, Monash University, Parkville, VIC, 3052, Australia., Mitchell A; School of Engineering, RMIT University, La Trobe Street, Melbourne, VIC, 3004, Australia., Ooi ASH; Department of Mechanical Engineering, Faculty of Engineering and Information Technology, The University of Melbourne, Melbourne, VIC, 3010, Australia., Hamilton JR; The Australian Centre for Blood Diseases, Monash University, Melbourne, VIC, 3004, Australia., Nesbitt WS; The Australian Centre for Blood Diseases, Monash University, Melbourne, VIC, 3004, Australia. warwick.nesbitt@monash.edu.
المصدر: BMC biology [BMC Biol] 2022 Mar 24; Vol. 20 (1), pp. 73. Date of Electronic Publication: 2022 Mar 24.
نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: BioMed Central Country of Publication: England NLM ID: 101190720 Publication Model: Electronic Cited Medium: Internet ISSN: 1741-7007 (Electronic) Linking ISSN: 17417007 NLM ISO Abbreviation: BMC Biol Subsets: MEDLINE
أسماء مطبوعة: Original Publication: [London] : BioMed Central, c2003-
مواضيع طبية MeSH: Platelet Activation* , Thrombosis*, Blood Platelets/metabolism ; Hemodynamics ; Humans ; Ion Channels ; Stress, Mechanical ; von Willebrand Factor/metabolism
مستخلص: Background: Supraphysiological hemodynamics are a recognized driver of platelet activation and thrombosis at high-grade stenosis and in blood contacting circulatory support devices. However, whether platelets mechano-sense hemodynamic parameters directly in free flow (in the absence of adhesion receptor engagement), the specific hemodynamic parameters at play, the precise timing of activation, and the signaling mechanism(s) involved remain poorly elucidated.
Results: Using a generalized Newtonian computational model in combination with microfluidic models of flow acceleration and quasi-homogenous extensional strain, we demonstrate that platelets directly mechano-sense acute changes in free-flow extensional strain independent of shear strain, platelet amplification loops, von Willebrand factor, and canonical adhesion receptor engagement. We define an extensional strain sensing "mechanosome" in platelets involving cooperative Ca 2+ signaling driven by the mechanosensitive channel Piezo1 (as the primary strain sensor) and the fast ATP gated channel P2X1 (as the secondary signal amplifier). We demonstrate that type II PI3 kinase C2α activity (acting as a "clutch") couples extensional strain to the mechanosome.
Conclusions: Our findings suggest that platelets are adapted to rapidly respond to supraphysiological extensional strain dynamics, rather than the peak magnitude of imposed wall shear stress. In the context of overall platelet activation and thrombosis, we posit that "extensional strain sensing" acts as a priming mechanism in response to threshold levels of extensional strain allowing platelets to form downstream adhesive interactions more rapidly under the limiting effects of supraphysiological hemodynamics.
(© 2022. The Author(s).)
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فهرسة مساهمة: Keywords: Extensional strain; Hemodynamics; Mechanotransduction; Platelet
المشرفين على المادة: 0 (Ion Channels)
0 (PIEZO1 protein, human)
0 (von Willebrand Factor)
تواريخ الأحداث: Date Created: 20220325 Date Completed: 20220414 Latest Revision: 20220414
رمز التحديث: 20240628
مُعرف محوري في PubMed: PMC8944166
DOI: 10.1186/s12915-022-01274-7
PMID: 35331224
قاعدة البيانات: MEDLINE
الوصف
تدمد:1741-7007
DOI:10.1186/s12915-022-01274-7