Evidence for cross-talk between glycoprotein VI and Gi-coupled receptors during collagen-induced platelet aggregation.

摘要: Collagen-induced platelet aggregation is a complex process and involves synergistic action of integrins, immunoglobulin (Ig)-like receptors, G-protein–coupled receptors their ligands, most importantly collagen itself, thromboxane A2(TXA2), adenosine diphosphate (ADP). The precise role each these receptor systems in the overall processes activation aggregation, however, still poorly defined. Among expressed on platelets, glycoprotein (GP) VI has been identified to play crucial collagen-induced activation. GPVI associated with FcRγ chain, which serves as signal transducing unit complex. It well known that clustering by highly specific agonists results irreversible but it unclear whether same effect receptor. This study shows platelets from Gαq-deficient mice, despite severely impaired response collagen, normally aggregate GPVI, suggesting this not be principal mechanism activates platelets. On other hand, dimerization monoclonal antibody (JAQ1), itself did induce provided sufficient stimulus potentiate responses Gi-coupled, Gq-coupled, agonists. combination JAQ1 adrenaline or ADP, serotonin, resulted αIIbβ3-dependent occurred without intracellular calcium mobilization shape change absence Gαq P2Y1 Together, provide evidence for cross-talk between (dimerized) Gi-coupled during aggregation.