Publication: Platelet ad hesion receptors and (patho)physiological thrombus formation
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Date
2001
Authors
Andrews, R.K. ; Shen, Y. ; Gardiner, E.E. ; Berndt, M.C.
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Publisher
Murcia : F. Hernández
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DOI
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info:eu-repo/semantics/article
Description
Abstract
In thrombus formation associated with
hemostasis or thrombotic disease, blood platelets first
undergo a rapid transition from a circulating state to an
adherent state, followed by activation and aggregation.
Under flow conditions in the bloodstream, this process
potentially involves platelet-platelet, plateletendothelium,
platelet-subendothelial matrix, and
platelet-leukocyte interactions. Specific adhesion
receptors on platelets mediate these interactions, by
engaging counter-receptors on other cells, or noncellular
ligands in the plasma or matrix. The
glycoprotein (GP) Ib-IX-V complex on platelets initiates
adhesion at high shear stress by binding the adhesive
ligand, von Willebrand Factor (vWF). GP Ib-IX-V may
also mediate platelet-endothelium or platelet-leukocyte
adhesion, by recognition of P-selectin or Mac-1,
respectively. Other membrane glycoproteins, such as the
collagen receptor GP VI, may trigger platelet activation
at low shear rates. Engagement of GP Ib-IX-V or GP VI
leads ultimately to platelet aggregation mediated by the
integrin, aIIbB3 (GP IIb-IIIa). This review will focus on
recent advances in understanding structure-activity
relationships of GP Ib-IX-V, its role in initiating
thrombus formation, and its emerging relationships with
other vascular cell adhesion receptors.
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