Key result
Mice lacking the PGE2 receptor subtype 3 (EP3-/-) exhibited significantly prolonged bleeding time and reduced mortality and lung thrombus formation when challenged with arachidonic acid.
Population
Mice lacking the PGE2 receptor subtype 3 (EP3-/- mice) and murine platelets
Comparison
Genetic deletion of EP3 receptor and in vitro… vs Wild-type mice/platelets (implied)
Design
Preclinical
Authors
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EP3 deletion attenuates thrombosis in mice; leaves open whether selective antagonism is antithrombotic in humans.
PGE2 potentiates platelet aggregation via the EP3 receptor, and its absence in mice leads to increased bleeding tendency and decreased susceptibility to thromboembolism.
Ma et al. (2001) studied Hemostasis and thromboembolism. EP3 receptor knockout vs. Wild-type mice was evaluated on Bleeding time, mortality, and thrombus formation. Mice lacking the PGE2 receptor subtype 3 (EP3-/-) exhibited significantly prolonged bleeding time and reduced mortality and lung thrombus formation when challenged with arachidonic acid.
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