Deficiency or inhibition of Gas6 causes platelet dysfunction and protects mice against thrombosis View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2001-02

AUTHORS

Anne Angelillo-Scherrer, Pablo Garcia de Frutos, Cristina Aparicio, Els Melis, Pierre Savi, Florea Lupu, Jef Arnout, Mieke Dewerchin, Marc F. Hoylaerts, Jean-Marc Herbert, Désiré Collen, Björn Dahlbäck, Peter Carmeliet

ABSTRACT

The growth arrest-specific gene 6 product (Gas6) is a secreted protein related to the anticoagulant protein S but its role in hemostasis is unknown. Here we show that inactivation of the Gas6 gene prevented venous and arterial thrombosis in mice, and protected against fatal collagen/epinephrine-induced thrombo embolism. Gas6-/- mice did not, however, suffer spontaneous bleeding and had normal bleeding after tail clipping. In addition, we found that Gas6 antibodies inhibited platelet aggregation in vitro and protected mice against fatal thrombo embolism without causing bleeding in vivo. Gas6 amplified platelet aggregation and secretion in response to known agonists. Platelet dysfunction in Gas6-/- mice resembled that of patients with platelet signaling transduction defects. Thus, Gas6 is a platelet-response amplifier that plays a significant role in thrombosis. These findings warrant further evaluation of the possible therapeutic use of Gas6 inhibition for prevention of thrombosis. More... »

PAGES

215

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/84667

DOI

http://dx.doi.org/10.1038/84667

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1044414965

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/11175853


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