期刊
BLOOD
卷 117, 期 15, 页码 4125-4133出版社
AMER SOC HEMATOLOGY
DOI: 10.1182/blood-2010-08-301366
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资金
- National Institutes of Health (NIH
- Bethesda, MD) National Heart, Lung and Blood Institute [HL26441, P01-HL55552]
- Biotechnology and Biological Sciences Research Council (Wiltshire, United Kingdom)
- NIH [GM091739]
- Foundation Leducq (Paris, France)
- Conselho Nacional de Desenvolvimento Cientifico e Tecnologico (Brasilia, Brazil)
- Biotechnology and Biological Sciences Research Council [BB/E52708X/1] Funding Source: researchfish
- BBSRC [BB/E52708X/1] Funding Source: UKRI
The microvasculature assumes an inflammatory and procoagulant state in a variety of different diseases, including sickle cell disease (SCD), which may contribute to the high incidence of ischemic stroke in these patients. This study provides evidence for accelerated thrombus formation in arterioles and venules in the cerebral vasculature of mice that express hemoglobin-S (beta(s) mice). Enhanced microvascular thrombosis in beta(s) mice was blunted by immunologic or genetic interventions that target tissue factor, endothelial protein C receptor, activated protein C, or thrombin. Platelets from beta(s) mice also exhibited enhanced aggregation velocity after stimulation with thrombin but not ADP. Neutropenia also protected against the enhanced thrombosis response in beta(s) mice. These results indicate that the cerebral microvasculature is rendered vulnerable to thrombus formation in beta(s) mice via a neutrophil-dependent mechanism that is associated with an increased formation of and enhanced platelet sensitivity to thrombin. (Blood. 2011; 117(15):4125-4133)
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