Key result
Disruption of lipid rafts by cholesterol extraction blunted platelet aggregation and calcium increase in response to TXA2 analogs, indicating TXA2 receptors depend on lipid rafts.
The localization of TXA2 receptors to lipid rafts is essential for normal platelet activation and functional responses to TXA2.
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Lipid raft integrity may be required for TXA2-mediated platelet activation; leaves open whether raft-targeted interventions could modulate thrombosis in vivo.
We have investigated the presence of thromboxane A2 (TXA2) receptor associated with lipid rafts in human platelets and the regulation of platelet function in response to TXA2 receptor agonists when lipid rafts are disrupted by cholesterol extraction. Platelet aggregation with TXA2 analogs U46619 and IBOP was almost blunted in cholesterol-depleted platelets, as well as αIIbβ3 integrin activation and P-selectin exposure. Raft disruption also inhibited TXA2-induced cytosolic calcium increase and nucleotide release, ruling out an implication of P2Y12 receptor. An important proportion of TXA2 receptor (40%) was colocalized at lipid rafts. The presence of the TXA2 receptor associated with lipid rafts in platelets is important for functional platelet responses to TXA2.
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Moscardó et al. (2014) studied this question. Cholesterol extraction (lipid raft disruption) vs. Intact lipid rafts was evaluated on Platelet functional responses to TXA2 analogs. Disruption of lipid rafts by cholesterol extraction blunted platelet aggregation and calcium increase in response to TXA2 analogs, indicating TXA2 receptors depend on lipid rafts.
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