Abstract
Platelet activation is crucial for normal hemostasis to arrest bleeding following vascular injury. However, excessive platelet activation in narrowed atherosclerotic blood vessels that are subject to high shear forces may initiate the onset of arterial thrombosis. When platelets come into contact with, and adhere to collagen exposed by damaged endothelium, they undergo morphological and functional changes necessary to generate a platelet-rich thrombus. This process is complex and involves precise co-ordination of various signaling pathways which lead to firm platelet adhesion to sites of tissue damage, release of granule contents from activated platelets, platelet shape change, platelet aggregation and subsequent thrombus formation and consolidation. Induction of tyrosine phosphorylation of key signaling molecules has emerged as a critical event central to stimulatory signaling pathways that generate platelet activation, but is an essential component associated with regulatory pathways that limit the extent of platelet activation. Understanding mechanisms that regulate platelet activation may contribute to the development of novel therapeutics that control common vascular diseases such as myocardial infarction and ischaemic stroke.
Keywords: GPIb-IX-V, Collagen Receptor, Signal transduction, ITAM motifs, Src-homology 2 domain containing phosphatase-1, (SHP-1)
Current Drug Targets
Title: Phosphotyrosine Signaling in Platelets: Lessons for Vascular Thrombosis
Volume: 7 Issue: 10
Author(s): Janet L. K. Wee and Denise E. Jackson
Affiliation:
Keywords: GPIb-IX-V, Collagen Receptor, Signal transduction, ITAM motifs, Src-homology 2 domain containing phosphatase-1, (SHP-1)
Abstract: Platelet activation is crucial for normal hemostasis to arrest bleeding following vascular injury. However, excessive platelet activation in narrowed atherosclerotic blood vessels that are subject to high shear forces may initiate the onset of arterial thrombosis. When platelets come into contact with, and adhere to collagen exposed by damaged endothelium, they undergo morphological and functional changes necessary to generate a platelet-rich thrombus. This process is complex and involves precise co-ordination of various signaling pathways which lead to firm platelet adhesion to sites of tissue damage, release of granule contents from activated platelets, platelet shape change, platelet aggregation and subsequent thrombus formation and consolidation. Induction of tyrosine phosphorylation of key signaling molecules has emerged as a critical event central to stimulatory signaling pathways that generate platelet activation, but is an essential component associated with regulatory pathways that limit the extent of platelet activation. Understanding mechanisms that regulate platelet activation may contribute to the development of novel therapeutics that control common vascular diseases such as myocardial infarction and ischaemic stroke.
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Cite this article as:
K. Wee L. Janet and Jackson E. Denise, Phosphotyrosine Signaling in Platelets: Lessons for Vascular Thrombosis, Current Drug Targets 2006; 7 (10) . https://dx.doi.org/10.2174/138945006778559265
DOI https://dx.doi.org/10.2174/138945006778559265 |
Print ISSN 1389-4501 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-5592 |
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