P2X1-initiated p38 signalling enhances thromboxane A2-induced platelet secretion and aggregation
P2X1-initiated p38 signalling enhances thromboxane A2-induced platelet secretion and aggregation
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DOI：
10.1160/th13-09-0726
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发表时间：
2014-07-01
影响因子：
6.7
通讯作者：
Hu, Hu
中科院分区：
文献类型：
--
作者：
Huang, Zhangsen;Liu, Pu;Hu, Hu
由活化的血小板释放的ATP可以作为正反馈，通过激活P2 X1受体来放大血小板反应。然而，P2 X（1）活性如何影响血栓素A（2）（TXA（2））刺激的血小板功能反应尚未确定。我们的目的是阐明P2 X（1）参与TXA（2）诱导的血小板分泌和聚集的分子机制。1 μ M NF 449抑制P2 X（1）可抑制低浓度TXA（2）类似物U46619（0.3 μ M）诱导的血小板P-选择素表达（32.0 ± 2.0%vs 43.4 ± 3.0%; n=5; p
ATP released by activated platelets can serve as a positive feedback, machinery to amplify platelet responses by activating P2X1 receptors. It has, however, not been defined how P2X(1) activities influence thromboxane A(2) (TXA(2))-stimulated platelet functional responses. Our aim was to elaborate the molecular mechanisms of P2X(1) engagements in TXA(2)-induced platelet secretion and aggregation. P2X(1) inhibition by 1 mu M NF449 inhibited platelet P-selectin expression induced by a low concentration of the TXA(2) analogue U46619 (0.3 mu M) (32.0 +/- 2.0% vs 43.4 +/- 3.0%; n=5; p