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Blood, 1 September 2001, Vol. 98, No. 5, pp. 1456-1463
HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY
Platelet endothelial cell adhesion molecule-1 is a negative
regulator of platelet-collagen interactions
Karen L. Jones,
Sascha C. Hughan,
Sacha M. Dopheide,
Richard W. Farndale,
Shaun P. Jackson, and
Denise E. Jackson
From the Division of Haematology, Hanson Centre for
Cancer Research, IMVS, Adelaide; the Department of Medicine, Australian
Centre for Blood Diseases, Monash University, Box Hill Hospital,
Victoria, Australia; and the Department of Biochemistry, University of
Cambridge, United Kingdom.
The functional importance of platelet endothelial cell adhesion
molecule-1 (PECAM-1/CD31) in platelets is unclear. Because PECAM-1
represents a newly assigned immunoglobulin-ITIM superfamily member
expressed on the surface of platelets, it was hypothesized that it may
play an important regulatory role in modulating ITAM-bearing receptors
such as collagen (GP)VI receptor and Fc RIIA. To examine the
functional role of PECAM-1 in regulating platelet-collagen interactions, 2 different approaches were applied using recombinant human PECAM-1-immunoglobulin chimeras and platelets derived from PECAM-1-deficient mice. Stimulation of platelets by collagen-, (GP)VI-selective agonist, collagen-related peptide (CRP)-, and PECAM-1-immunoglobulin chimera induced tyrosine phosphorylation of
PECAM-1 in a time- and dose-dependent manner. Activation of PECAM-1
directly through the addition of soluble wild-type
PECAM-1-immunoglobulin chimera, but not mutant K89A
PECAM-1-immunoglobulin chimera that prevents homophilic binding, was
found to inhibit collagen- and CRP-induced platelet aggregation.
PECAM-1-deficient platelets displayed enhanced platelet aggregation
and secretion responses on stimulation with collagen and CRP, though
the response to thrombin was unaffected. Under conditions of flow,
human platelet thrombus formation on a collagen matrix was reduced in a
dose-dependent manner by human PECAM-1-immunoglobulin chimera.
Platelets derived from PECAM-1-deficient mice form larger thrombi when
perfused over a collagen matrix under flow at a shear rate of 1800 seconds 1 compared to wild-type mice. Collectively, these
results indicate that PECAM-1 serves as a physiological negative
regulator of platelet-collagen interactions that may function to
negatively limit growth of platelet thrombi on collagen surfaces.
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