Key result
Prostaglandins induce platelet aggregation by combining with a specific endoperoxide receptor, and arachidonate metabolism is necessary for collagen-induced release of lysosomal enzymes.
May inform endoperoxide receptor targeting in platelets; leaves open clinical translation to antithrombotic therapy.
The effects of PGG2 and PGH2 on platelets are mimicked by synthetic PG analogues in which the nature and specificity of the substituents on carbons 11 and 15 (or 16) are important determinants of reactivity. Arachidonic acid and stimulatory PGs induce secretion of platelet dense granule and alpha granule constituents, but not lysomal constituents, although arachidonate metabolism is necessary for collagen-induced release of lysosomal enzymes. NO164 acts on platelets as an endoperoxide antagonist: Trimethoquinol acts as an endoperoxide and TxA2 antagonist. PGs induce platelet aggregation by combining with a specific (endoperoxide) receptor.
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Euan MacIntyre (2009) studied Platelet function. Prostaglandins and analogues was evaluated on Platelet aggregation and degranulation. Prostaglandins induce platelet aggregation by combining with a specific endoperoxide receptor, and arachidonate metabolism is necessary for collagen-induced release of lysosomal enzymes.
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