Reference : ATP Augments von Willebrand Factor-dependent Shear-induced Platelet Aggregation through ...

	Document type :	Scientific journals : Article
	Discipline(s) :	Life sciences : Biochemistry, biophysics & molecular biology
	To cite this reference:	http://hdl.handle.net/2268/20355

Title :	ATP Augments von Willebrand Factor-dependent Shear-induced Platelet Aggregation through Ca2+-Calmodulin and Myosin Light Chain Kinase Activation
Language :	English
Author, co-author :	Oury, Cécile [Katholieke Universiteit Leuven - KUL > Molecular and Cellular Medicine > CMVB > >]
	Sticker, Elsie [Katholieke Universiteit Leuven - KUL > Departement of Molecular and Cellular Medicine > CMVB > >]
	Cornelissen, Heidi [Katholieke Universiteit Leuven - KUL > Department of Molecular and Cellular Medicine > CMVB > >]
	De Vos, Rita [Katholieke Universiteit Leuven - KUL > Department of Medical Diagnostic Sciences > Morphology and Molecular Pathology Section > >]
	Vermylen, Jos [Katholieke Universiteit Leuven - KUL > Department of Molecular and Cellular Medicine > CMVB > >]
	Hoylaerts, Marc F [Katholieke Universiteit Leuven - KUL > Department of Molecular and Cellular Medicine > CMVB > >]
Publication date :	2004
Journal title :	Journal of Biological Chemistry
Publisher :	American Society for Biochemistry and Molecular Biology
Audience :	International
ISSN :	0021-9258
e-ISSN :	1083-351X
City :	Baltimore
Country :	MD
Keywords :	[en] platelets ; shear stress ; signaling pathway
Abstract :	[en] Shear stress triggers von Willebrand factor (VWF) binding to platelet glycoprotein Ibalpha and subsequent integrin alpha(IIb)beta(3)-dependent platelet aggregation. Concomitantly, nucleotides are released from plateletdense granules, and ADP is known to contribute to shear-induced platelet aggregation (SIPA). This study shows that ATP also contributes to SIPA. The ATP-gated P2X(1) ion channel induces MLC-mediated cytoskeletal rearrangements that increases platelet degranulation during VWF-triggered platelet activation.
Permalink :	http://hdl.handle.net/2268/20355

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