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Int. J. Mol. Sci. 2017, 18(6), 1238; doi:10.3390/ijms18061238

Syk Activity Is Dispensable for Platelet GP1b-IX-V Signaling

1
Department of Physiology, Temple University, Room 414 MRB, 3420 N. Broad Street, Philadelphia, PA 19140, USA
2
Sol Sherry Thrombosis Research Center, Temple University, Room 414 MRB, 3420 N. Broad Street, Philadelphia, PA 19140, USA
3
Department of Pharmacology, Temple University School of Medicine, Philadelphia, PA 19140, USA
*
Author to whom correspondence should be addressed.
Academic Editor: Denise Jackson
Received: 31 March 2017 / Revised: 31 May 2017 / Accepted: 2 June 2017 / Published: 9 June 2017
(This article belongs to the Special Issue Mechanisms of Platelet Thrombus Formation)
View Full-Text   |   Download PDF [1659 KB, uploaded 9 June 2017]   |  

Abstract

The binding of von Willebrand factor (VWF) to the platelet membrane glycoprotein 1b-IX (GP1b-IX) leads to activation of platelets. GP1b was shown to signal via the FcRγ-ITAM (Fc Receptor γ-Immunoreceptor tyrosine-based activation motif) pathway, activating spleen tyrosine kinase (Syk) and other tyrosine kinases. However, there have been conflicting reports regarding the role of Syk in GP1b signaling. In this study, we sought to resolve these conflicting reports and clarify the role of Syk in VWF-induced platelet activation. The inhibition of Syk with the selective Syk inhibitors, OXSI-2 and PRT-060318, did not inhibit VWF-induced platelet adhesion, agglutination, aggregation, or secretion. In contrast, platelets stimulated with the Glycoprotein VI (GPVI) agonist, collagen-related peptide (CRP), failed to cause any aggregation or secretion in presence of the Syk inhibitors. Furthermore, GP1b-induced platelet signaling was unaffected in the presence of Syk inhibitors, but GPVI-induced signaling was abolished under similar conditions. Thus, we conclude that Syk kinase activity does not play any functional role downstream of GP1b-mediated platelet activation. View Full-Text
Keywords: platelets; GP1b receptor; von Willebrand factor (VWF); spleen tyrosine kinase (Syk) platelets; GP1b receptor; von Willebrand factor (VWF); spleen tyrosine kinase (Syk)
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MDPI and ACS Style

Badolia, R.; Kostyak, J.C.; Dangelmaier, C.; Kunapuli, S.P. Syk Activity Is Dispensable for Platelet GP1b-IX-V Signaling. Int. J. Mol. Sci. 2017, 18, 1238.

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