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Related Collections Hemostasis, Thrombosis, and Vascular Biology Red Cells Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 1 June 2002, Vol. 99, No. 11, pp. 3978-3984 HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY Platelet-erythrocyte interactions enhance IIb3 integrin receptor activation and P-selectin expression during platelet recruitment: down-regulation by aspirin ex vivo Juana Vallés, M. Teresa Santos, Justo Aznar, Marcial Martínez, Antonio Moscardó, Marta Piñón, M. Johan Broekman, and Aaron J. Marcus From the Research Center and Department of Clinical Pathology, University Hospital La Fe, Valencia, Spain; Division of Hematology and Medical Oncology, Department of Medicine, VA New York Harbor Healthcare System, New York, NY; and Division of Hematology and Medical Oncology, Departments of Medicine and Pathology, Weill Medical College of Cornell University, New York, NY. Activated platelets release biologically active compounds, which then recruit additional platelets into an evolving thrombus. We studied activation of IIb3 and exposure of P-selectin on platelets recruited by releasates obtained from collagen-treated platelets and evaluated modifications in prothrombotic effects of releasates induced by platelet-erythrocyte interactions and aspirin treatment. Releasates from collagen-stimulated platelets induced IIb3 activation and P-selectin exposure (monitored by flow cytometry using fluorescein isothiocyanate-PAC-1 and phycoerythrin-CD62 antibodies). These responses were markedly amplified by releasates from combined platelet-erythrocyte suspensions. This finding demonstrates a novel mechanism(s) by which erythrocytes intensify platelet aggregability and mediate increased platelet recruitment. Because P-selectin and IIb3 are potential sites for platelet-leukocyte interactions, erythrocytes may also modulate leukocyte recruitment. Following aspirin ingestion both the recruiting capacity of platelet releasates and erythrocyte-induced amplification of platelet recruitment were down-regulated. These events represent an additional antithrombotic property of aspirin. We also examined the possibility that arachidonic acid, or eicosanoids derived therefrom, can induce a prothrombotic activity of erythrocytes. The TXA2-analog U46 619 and free arachidonate, but not PGI2 or 12-HETE, induced increases in cytosolic Ca++ and promoted phosphatidylserine (PS) exposure on a subpopulation of erythrocytes. PS exposure and increases in erythrocyte [Ca++]i are associated with enhanced procoagulant activity, increased endothelial adhesion, and reduced erythrocyte deformability. Our findings, therefore, suggest that TXA2 and arachidonic acid, derived from activated platelets, induce a prothrombotic phenotype on erythrocytes in proximity. 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