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Related Collections Hemostasis, Thrombosis, and Vascular Biology Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 15 June 2001, Vol. 97, No. 12, pp. 3829-3835 HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY Evidence for cross-talk between glycoprotein VI and Gi-coupled receptors during collagen-induced platelet aggregation Bernhard Nieswandt, Wolfgang Bergmeier, Anita Eckly, Valerie Schulte, Philippe Ohlmann, Jean-Pierre Cazenave, Hubert Zirngibl, Stefan Offermanns, and Christian Gachet From the Department of Molecular Oncology, General Surgery, Witten/Herdecke University, Wuppertal, Germany; INSERM U.311, Etablissement Français du Sang-Alsace, Strasbourg Cedex, France; and Department of Molecular Pharmacology, University of Heidelberg, Heidelberg, Germany. Collagen-induced platelet aggregation is a complex process and involves synergistic action of integrins, immunoglobulin (Ig)-like receptors, G-protein-coupled receptors and their ligands, most importantly collagen itself, thromboxane A2 (TXA2), and adenosine diphosphate (ADP). The precise role of each of these receptor systems in the overall processes of activation and aggregation, however, is still poorly defined. Among the collagen receptors expressed on platelets, glycoprotein (GP) VI has been identified to play a crucial role in collagen-induced activation. GPVI is associated with the FcR chain, which serves as the signal transducing unit of the receptor complex. It is well known that clustering of GPVI by highly specific agonists results in platelet activation and irreversible aggregation, but it is unclear whether collagen has the same effect on the receptor. This study shows that platelets from Gq-deficient mice, despite their severely impaired response to collagen, normally aggregate on clustering of GPVI, suggesting this not to be the principal mechanism by which collagen activates platelets. On the other hand, dimerization of GPVI by a monoclonal antibody (JAQ1), which by itself did not induce aggregation, provided a sufficient stimulus to potentiate platelet responses to Gi-coupled, but not Gq-coupled, agonists. The combination of JAQ1 and adrenaline or ADP, but not serotonin, resulted in IIb3-dependent aggregation that occurred without intracellular calcium mobilization and shape change in the absence of Gq or the P2Y1 receptor. Together, these results provide evidence for a cross-talk between (dimerized) GPVI and Gi-coupled receptors during collagen-induced platelet aggregation. © 2001 by The American Society of Hematology.   CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? 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