Why the study?
Do TA-993 and its metabolite MB3 inhibit platelet activation induced by collagen and U-46619 in human platelets?
Do TA-993 and its metabolite MB3 inhibit platelet activation induced by collagen and U-46619 in human platelets?
TA-993 and its metabolite MB3 inhibit collagen-induced platelet activation partly by inhibiting TxA2 formation prior to cyclooxygenase, and inhibit U-46619-induced activation without blocking intracellular Ca2+ increase.
Should not yet change antiplatelet practice; leaves open translation of TA-993/MB3 effects to human thrombosis prevention.
In the present study, we investigated the effects of TA-993 and its metabolite MB3 on platelet activation in vitro. TA-993 and MB3 concentration-dependently inhibited platelet aggregation and ATP release induced by collagen in human platelets. Thromboxane (Tx) A2 formation, as determined by the production of TxB2, and the increase in intracellular Ca2+ concentration ([Ca2+]i) were also suppressed by TA-993 and MB3. TA-993 and MB3 did not inhibit TxA2 formation caused by arachidonic acid. These results suggest that the inhibition of platelet activation by TA-993 and MB3 is partly mediated by an inhibition of TxA2 formation at a step prior to cyclooxygenase. Furthermore, TA-993 and MB3 inhibited U-46619-induced platelet aggregation without blockade of the increase in [Ca2+]i, suggesting that they are likely to exert some additional effects on the intracellular events induced by Ca2+.
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Katoh et al. (2001) studied this question.
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