Defective platelet activation in Gαq-deficient mice

Stefan Offermanns, Christopher F. Toombs, Yi-Hui Hu and Melvin I. Simon ()
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Stefan Offermanns: Freie Universität Berlin
Christopher F. Toombs: Amgen Inc.
Yi-Hui Hu: California Institute of Technology
Melvin I. Simon: Amgen Inc.

Nature, 1997, vol. 389, issue 6647, 183-186

Abstract: Abstract Platelets are small disc-shaped cell fragments which undergo a rapid transformation when they encounter vascular damage. They become more spherical and extrude pseudopodia, their fibrinogen receptors are activated, causing them to aggregate, they release their granule contents, and eventually form a plug which is responsible for primary haemostasis1. Activation of platelets is also implicated in the pathogenesis of unstable angina, myocardial infarction and stroke2,3. Here we show that platelets from mice deficient in the α-subunit of the heterotrimeric guanine-nucleotide-binding protein Gq are unresponsive to a variety of physiological platelet activators. As a result, Gαq-deficient mice have increased bleeding times and are protected from collagen and adrenaline-induced thromboembolism. We conclude that Gαq is essential for the signalling processes used by different platelet activators and that it cannot be replaced by Gαi or the βγ subunits of the heterotrimeric G proteins. Gαq may thus be a new target for drugs designed to block the activation of platelets.

Date: 1997
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DOI: 10.1038/38284

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