Understanding the role of prostaglandin E2 in regulating human platelet activity in health and disease

Abstract The platelet thrombus is the major pathologic entity in acute coronary syndromes, and antiplatelet agents are a mainstay of therapy. However, individual patient responsiveness to current antiplatelet drugs is variable, and all drugs carry a risk of bleeding. An understanding of the complex...

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Bibliographic Details
Published in:Thrombosis research 2015-09, Vol.136 (3), p.493-503
Main Authors: Friedman, Eitan A, Ogletree, Martin L, Haddad, Elias V, Boutaud, Olivier
Format: Article
Language:English
Subjects:
Animals
Antiplatelet agent
Blood Platelets - metabolism
Dinoprostone - metabolism
EP3 antagonist
Evidence-Based Medicine
Hematology, Oncology and Palliative Medicine
Humans
Mice
Models, Cardiovascular
Platelet Activation
platelet aggregation
platelet inhibitor
platelet reactivity regulation
prostaglandin E2
Species Specificity
Thrombosis - metabolism
Thrombosis - pathology
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Summary:Abstract The platelet thrombus is the major pathologic entity in acute coronary syndromes, and antiplatelet agents are a mainstay of therapy. However, individual patient responsiveness to current antiplatelet drugs is variable, and all drugs carry a risk of bleeding. An understanding of the complex role of Prostaglandin E2 (PGE2 ) in regulating thrombosis offers opportunities for the development of novel individualized antiplatelet treatment. However, deciphering the platelet regulatory function of PGE2 has long been confounded by non-standardized experimental conditions, extrapolation of murine data to humans, and phenotypic differences in PGE2 response. This review synthesizes past and current knowledge about PGE2 effects on platelet biology, presents a rationale for standardization of experimental protocols, and provides insight into a molecular mechanism by which PGE2 -activated pathways could be targeted for new personalized antiplatelet therapy to inhibit pathologic thrombosis without affecting hemostasis.
ISSN:0049-3848
1879-2472
DOI:10.1016/j.thromres.2015.05.027