Endothelial Shear Stress and Platelet FcγRIIa Expression in Intracranial Atherosclerotic Disease

Intracranial atherosclerotic disease (ICAD) has been characterized by the degree of arterial stenosis and downstream hypoperfusion, yet microscopic derangements of endothelial shear stress at the luminal wall may be key determinants of plaque growth, vascular remodeling and thrombosis that culminate...

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Main Authors:	David S. Liebeskind, Jason D. Hinman, Naoki Kaneko, Hiroaki Kitajima, Tristan Honda, Adam H. De Havenon, Edward Feldmann, Raul G. Nogueira, Shyam Prabhakaran, Jose G. Romano, Peter W. Callas, David J. Schneider
Format:	Article
Language:	English
Published:	Frontiers Media S.A. 2021-02-01
Series:	Frontiers in Neurology
Subjects:	intracranial atherosclerosis stroke shear stress FcγRIIa receptor platelet activation and reactivity
Online Access:	https://www.frontiersin.org/articles/10.3389/fneur.2021.646309/full

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spelling	doaj-5a256ea05a604b098ca30533aecc1ee42021-02-25T07:09:28ZengFrontiers Media S.A.Frontiers in Neurology1664-22952021-02-011210.3389/fneur.2021.646309646309Endothelial Shear Stress and Platelet FcγRIIa Expression in Intracranial Atherosclerotic DiseaseDavid S. Liebeskind0Jason D. Hinman1Naoki Kaneko2Hiroaki Kitajima3Tristan Honda4Adam H. De Havenon5Edward Feldmann6Raul G. Nogueira7Shyam Prabhakaran8Jose G. Romano9Peter W. Callas10David J. Schneider11Department of Neurology, Neurovascular Imaging Research Core and UCLA Stroke Center, University of California, Los Angeles, Los Angeles, CA, United StatesDepartment of Neurology, Neurovascular Imaging Research Core and UCLA Stroke Center, University of California, Los Angeles, Los Angeles, CA, United StatesDepartment of Neurology, Neurovascular Imaging Research Core and UCLA Stroke Center, University of California, Los Angeles, Los Angeles, CA, United StatesDepartment of Neurology, Neurovascular Imaging Research Core and UCLA Stroke Center, University of California, Los Angeles, Los Angeles, CA, United StatesDepartment of Neurology, Neurovascular Imaging Research Core and UCLA Stroke Center, University of California, Los Angeles, Los Angeles, CA, United StatesDepartment of Neurology, University of Utah, Salt Lake City, UT, United StatesDepartment of Neurology, The University of Massachusetts Medical School-Baystate, Springfield, MA, United StatesDepartment of Neurology, Marcus Stroke & Neuroscience Center, Emory University School of Medicine, Atlanta, GA, United StatesDepartment of Neurology, The University of Chicago, Chicago, IL, United StatesDepartment of Neurology, University of Miami, Miami, FL, United StatesDepartment of Biostatistics, University of Vermont, Burlington, VT, United StatesDepartment of Medicine, Cardiovascular Research Institute, University of Vermont, Burlington, VT, United StatesIntracranial atherosclerotic disease (ICAD) has been characterized by the degree of arterial stenosis and downstream hypoperfusion, yet microscopic derangements of endothelial shear stress at the luminal wall may be key determinants of plaque growth, vascular remodeling and thrombosis that culminate in recurrent stroke. Platelet interactions have similarly been a principal focus of treatment, however, the mechanistic basis of anti-platelet strategies is largely extrapolated rather than directly investigated in ICAD. Platelet FcγRIIa expression has been identified as a potent risk factor in cardiovascular disease, as elevated expression markedly increases the risk of recurrent events. Differential activation of the platelet FcγRIIa receptor may also explain the variable response of individual patients to anti-platelet medications. We review existing data on endothelial shear stress and potential interactions with the platelet FcγRIIa receptor that may alter the evolving impact of ICAD, based on local pathophysiology at the site of arterial stenosis. Current methods for quantification of endothelial shear stress and platelet activation are described, including tools that may be readily adapted to the clinical realm for further understanding of ICAD.https://www.frontiersin.org/articles/10.3389/fneur.2021.646309/fullintracranial atherosclerosisstrokeshear stressFcγRIIa receptorplatelet activation and reactivity
collection	DOAJ
language	English
format	Article
sources	DOAJ
author	David S. Liebeskind Jason D. Hinman Naoki Kaneko Hiroaki Kitajima Tristan Honda Adam H. De Havenon Edward Feldmann Raul G. Nogueira Shyam Prabhakaran Jose G. Romano Peter W. Callas David J. Schneider
spellingShingle	David S. Liebeskind Jason D. Hinman Naoki Kaneko Hiroaki Kitajima Tristan Honda Adam H. De Havenon Edward Feldmann Raul G. Nogueira Shyam Prabhakaran Jose G. Romano Peter W. Callas David J. Schneider Endothelial Shear Stress and Platelet FcγRIIa Expression in Intracranial Atherosclerotic Disease Frontiers in Neurology intracranial atherosclerosis stroke shear stress FcγRIIa receptor platelet activation and reactivity
author_facet	David S. Liebeskind Jason D. Hinman Naoki Kaneko Hiroaki Kitajima Tristan Honda Adam H. De Havenon Edward Feldmann Raul G. Nogueira Shyam Prabhakaran Jose G. Romano Peter W. Callas David J. Schneider
author_sort	David S. Liebeskind
title	Endothelial Shear Stress and Platelet FcγRIIa Expression in Intracranial Atherosclerotic Disease
title_short	Endothelial Shear Stress and Platelet FcγRIIa Expression in Intracranial Atherosclerotic Disease
title_full	Endothelial Shear Stress and Platelet FcγRIIa Expression in Intracranial Atherosclerotic Disease
title_fullStr	Endothelial Shear Stress and Platelet FcγRIIa Expression in Intracranial Atherosclerotic Disease
title_full_unstemmed	Endothelial Shear Stress and Platelet FcγRIIa Expression in Intracranial Atherosclerotic Disease
title_sort	endothelial shear stress and platelet fcγriia expression in intracranial atherosclerotic disease
publisher	Frontiers Media S.A.
series	Frontiers in Neurology
issn	1664-2295
publishDate	2021-02-01
description	Intracranial atherosclerotic disease (ICAD) has been characterized by the degree of arterial stenosis and downstream hypoperfusion, yet microscopic derangements of endothelial shear stress at the luminal wall may be key determinants of plaque growth, vascular remodeling and thrombosis that culminate in recurrent stroke. Platelet interactions have similarly been a principal focus of treatment, however, the mechanistic basis of anti-platelet strategies is largely extrapolated rather than directly investigated in ICAD. Platelet FcγRIIa expression has been identified as a potent risk factor in cardiovascular disease, as elevated expression markedly increases the risk of recurrent events. Differential activation of the platelet FcγRIIa receptor may also explain the variable response of individual patients to anti-platelet medications. We review existing data on endothelial shear stress and potential interactions with the platelet FcγRIIa receptor that may alter the evolving impact of ICAD, based on local pathophysiology at the site of arterial stenosis. Current methods for quantification of endothelial shear stress and platelet activation are described, including tools that may be readily adapted to the clinical realm for further understanding of ICAD.
topic	intracranial atherosclerosis stroke shear stress FcγRIIa receptor platelet activation and reactivity
url	https://www.frontiersin.org/articles/10.3389/fneur.2021.646309/full
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Endothelial Shear Stress and Platelet FcγRIIa Expression in Intracranial Atherosclerotic Disease

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