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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2004;24:e181.)
© 2004 American Heart Association, Inc.

Letters to the Editor

Measurement of Platelet Collagen Receptor Density in Human Subjects

Frederick F. Samaha; Christopher Hibbard; Jay Sacks; Hong Chen; Michael A. Varello; Thomas George; Mark L. Kahn

Philadelphia Veterans Affairs Medical Center, (F.F.S., J.S., M.A.V., T.G.) and, Department of Medicine, (F.F.S., C.H., H.C., M.L.K.),, Division of Cardiovascular Disease,, University of Pennsylvania Health System, Philadelphia, Penn

An extract of the first 250 words of the full text is provided, because this article has no abstract.

To the Editor:

We are writing to provide data on a novel approach for measuring platelet collagen receptors in human subjects. Immediately after vascular injury, circulating platelets are exposed to collagen, a matrix protein that both supports platelet adhesion and activates platelets through platelet collagen receptors.¹ Collagen signals generated at a site of arterial vessel injury are therefore likely to be among the first platelet activating signals that generate the coronary thrombi responsible for myocardial infarction. The molecular basis of platelet collagen responses has recently been elucidated by the identification and characterization of two platelet collagen receptors: the immune receptor homologue glycoprotein VI (GPVI)² and the integrin 2ß1.³ GPVI is required for platelet activation in response to collagen,^4,5 whereas 2ß1 plays an accessory role to support platelet responses to immobilized collagen in the setting of high shear forces.⁶

Preliminary findings from both laboratory and clinical studies suggest that the surface density of the platelet collagen receptors GPVI and 2ß1 may regulate the degree of platelet activation by collagen and its clinical outcome.^7–11 Despite these preliminary findings, the precise role of platelet collagen receptor density as a risk factor for MI remains poorly understood, with the few reported studies yielding apparently contradictory results. A study examining the correlation of platelet GPVI receptor polymorphisms with surface receptor density in normal individuals found one common allele (associated with the coding region polymorphism T683C) that correlated with lower GPVI receptor density and reduced collagen-mediated platelet aggregation.⁸ In contrast, a study examining GPVI polymorphisms in . . . [Full Text of this Article]

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