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Blood, 15 September 2007, Vol. 110, No. 6, pp. 1879-1886. Prepublished online as a Blood First Edition Paper on June 4, 2007; DOI 10.1182/blood-2006-08-040980.
HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY Conversion of platelets from a proaggregatory to a proinflammatory adhesive phenotype: role of PAF in spatially regulating neutrophil adhesion and spreading1 Australian Centre for Blood Diseases (ACBD), Monash University and Baker Heart Research Institute, at Alfred Medical Research and Education Precinct, Prahran, Victoria, Australia; 2 National Institute for Biological Standards and Control, Potters Bar, United Kingdom; 3 Proteomic research group, Babraham Institute, Cambridge, United Kingdom
The ability of platelets to provide a highly reactive surface for the recruitment of other platelets and leukocytes to sites of vascular injury is critical for hemostasis, atherothrombosis, and a variety of inflammatory diseases. The mechanisms coordinating platelet-platelet and platelet-leukocyte interactions have been well defined and, in general, it is assumed that increased platelet activation correlates with enhanced reactivity toward other platelets and neutrophils. In the current study, we demonstrate a differential role for platelets in supporting platelet and neutrophil adhesive interactions under flow. We demonstrate that the conversion of spread platelets to microvesiculated procoagulant (annexin A5–positive [annexin A5+ve]) forms reduces platelet-platelet adhesion and leads to a paradoxical increase in neutrophil-platelet interaction. This enhancement in neutrophil adhesion and spreading is partially mediated by the proinflammatory lipid, platelet-activating factor (PAF). PAF production, unlike other neutrophil chemokines (IL-8, GRO-
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| Copyright © 2007 by American Society of Hematology Online ISSN: 1528-0020 | |||||||||
, NAP-2, IL-1ß) is specifically and markedly up-regulated in annexin A5+ve cells. Physiologically, this spatially controlled production of PAF plays an important role in localizing neutrophils on the surface of thrombi. These studies define for the first time a specific proinflammatory function for annexin A5+ve platelets. Moreover, they demonstrate an important role for platelet-derived PAF in spatially regulating neutrophil adhesion under flow. 
