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Exogenous modification of platelet membranes with the omega-3 fatty acids EPA and DHA reduces platelet procoagulant activity and thrombus formation.
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Exogenous modification of platelet membranes with the omega-3 fatty acids EPA and DHA reduces platelet procoagulant activity and thrombus formation.

Author: MK Larson Affiliation: Department of Biology, Augustana College, Sioux Falls, SD 57197, USA. mklarson@augie.eduGW TormoenLJ WeaverKJ LuepkeIA PatelAll authors
Edition/Format: Article Article : English
Publication:American journal of physiology. Cell physiology, 2013 Feb 1; 304(3): C273-9
Database:From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.
Other Databases: Elsevier
Summary:
Several studies have implicated the omega-3 fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) in inhibition of normal platelet function, suggesting a role for platelets in EPA- and DHA-mediated cardioprotection. However, it is unclear whether the cardioprotective mechanisms arise from alterations to platelet-platelet, platelet-matrix, or platelet-coagulation factor interactions. Our previous  Read more...
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Details

Document Type: Article
All Authors / Contributors: MK Larson Affiliation: Department of Biology, Augustana College, Sioux Falls, SD 57197, USA. mklarson@augie.edu; GW Tormoen; LJ Weaver; KJ Luepke; IA Patel; CE Hjelmen; NM Ensz; LS McComas; OJ McCarty
ISSN:0363-6143
DOI: 10.1152/ajpcell.00174.2012
Language Note: English
Unique Identifier: 826795200
Awards:

Abstract:

Several studies have implicated the omega-3 fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) in inhibition of normal platelet function, suggesting a role for platelets in EPA- and DHA-mediated cardioprotection. However, it is unclear whether the cardioprotective mechanisms arise from alterations to platelet-platelet, platelet-matrix, or platelet-coagulation factor interactions. Our previous results led us to hypothesize that EPA and DHA alter the ability of platelets to catalyze the generation of thrombin. We tested this hypothesis by exogenously modifying platelet membranes with EPA and DHA, which resulted in compositional changes analogous to increased dietary EPA and DHA intake. Platelets treated with EPA and DHA showed reductions in the rate of thrombin generation and exposure of platelet phosphatidylserine. In addition, treatment of platelets with EPA and DHA decreased thrombus formation and altered the processing of thrombin precursor proteins. Furthermore, treatment of whole blood with EPA and DHA resulted in increased occlusion time and a sharply reduced accumulation of fibrin under flow conditions. These results demonstrate that EPA and DHA inhibit, but do not eliminate, the ability of platelets to catalyze thrombin generation in vitro. The ability of EPA and DHA to reduce the procoagulant function of platelets provides a possible mechanism behind the cardioprotective phenotype in individuals consuming high levels of EPA and DHA.
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