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Research Article Free access | 10.1172/JCI115468

von Willebrand factor binding to platelet GpIb initiates signals for platelet activation.

M H Kroll, T S Harris, J L Moake, R I Handin, and A I Schafer

Houston Veterans Affairs Medical Center, Baylor College of Medicine, Texas 77030.

Find articles by Kroll, M. in: PubMed | Google Scholar

Houston Veterans Affairs Medical Center, Baylor College of Medicine, Texas 77030.

Find articles by Harris, T. in: PubMed | Google Scholar

Houston Veterans Affairs Medical Center, Baylor College of Medicine, Texas 77030.

Find articles by Moake, J. in: PubMed | Google Scholar

Houston Veterans Affairs Medical Center, Baylor College of Medicine, Texas 77030.

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Houston Veterans Affairs Medical Center, Baylor College of Medicine, Texas 77030.

Find articles by Schafer, A. in: PubMed | Google Scholar

Published November 1, 1991 - More info

Published in Volume 88, Issue 5 on November 1, 1991
J Clin Invest. 1991;88(5):1568–1573. https://doi.org/10.1172/JCI115468.
© 1991 The American Society for Clinical Investigation
Published November 1, 1991 - Version history
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Abstract

The hypothesis that von Willebrand factor (vWF) binding to platelet membrane glycoprotein Ib (GpIb) initiates intracellular pathways of platelet activation was studied. We measured the biochemical responses of intact human platelets treated with ristocetin plus vWF multimers purified from human cryoprecipitate. vWF plus ristocetin causes the breakdown of phosphatidylinositol 4,5-bisphosphate, the production of phosphatidic acid (PA), the activation of protein kinase C (PKC), increase of ionized cytoplasmic calcium ([Ca2+]i), and the synthesis of thromboxane A2. PA production, PKC activation, and the rise of [Ca2+]i stimulated by the ristocetin-induced binding of vWF multimers to platelets are inhibited by an anti-GpIb monoclonal antibody, but are unaffected by anti-GpIIb-IIIa monoclonal antibodies. Indomethacin also inhibits these responses without impairing platelet aggregation induced by vWF plus ristocetin. These results indicate that vWF binding to platelets initiates specific intraplatelet signaling pathways. The mechanism by which this occurs involves an arachidonic acid metabolite-dependent activation of phospholipase C after vWF binding to platelet membrane GpIb. This signal then causes PKC activation and increases of [Ca2+]i, which promote platelet secretion and potentiate aggregation.

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