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首页> 外文期刊>Platelets >Actin polymerisation regulates thrombin-evoked Ca(2+) signalling after activation of PAR-4 but not PAR-1 in human platelets.
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Actin polymerisation regulates thrombin-evoked Ca(2+) signalling after activation of PAR-4 but not PAR-1 in human platelets.

机译：肌动蛋白聚合调节人血小板中的PAR-4激活但不激活PAR-1后调节凝血酶诱发的Ca（2+）信号传导。

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The role of actin polymerisation in regulating thrombin-evoked Ca(2+) signalling was investigated in human platelets. We have previously reported that cytochalasin D (Cyt D) inhibits thapsigargin-evoked store-operated Ca(2+) entry (SOCE), which is believed to contribute a major component of thrombin-evoked Ca(2+) entry in platelets. In contrast, Cyt D increased thrombin-evoked Ca(2+) entry to 147.5 +/- 9.2% and Sr(2+) entry to 134.2 +/- 6.4% of control. Similar results were obtained with latrunculin A. This potentiation was not affected if protein kinase C was inhibited using Ro-31-8220, suggesting that it did not involve PKC-dependent non-capacitative Ca(2+) entry. Ca(2+) entry evoked by the PAR-4 agonist, AYPGKF, was increased to 133.7 +/- 12.8% of control by Cyt D, whereas Ca(2+) signalling evoked by the PAR-1 agonist, SFLLRN, was unaffected. The PAR-4 antagonist, tcY-NH(2), abolished the effect of Cyt D on thrombin-evoked Ca(2+) entry. Biotinylation of cell-surface proteins showed that PAR-4 was internalised after stimulation by thrombin. Cyt D reduced this internalisation. These data suggest that Cyt D prevents the internalisation of PAR-4, which may lead to prolonged signalling from this receptor. This may mask a direct effect of Cyt D on the activation of SOCE after the activation of PAR-4.
机译：在人类血小板中研究了肌动蛋白聚合在调节凝血酶诱发的Ca（2+）信号传导中的作用。我们之前已经报道过，细胞松弛素D（Cyt D）抑制毒胡萝卜素诱发的存储操纵性Ca（2+）进入（SOCE），据信这是血小板中凝血酶诱发的Ca（2+）进入的主要成分。相比之下，Cyt D增加凝血酶诱发的Ca（2+）进入控制的147.5 +/- 9.2％和Sr（2+）进入控制的134.2 +/- 6.4％。 latrunculin A获得了类似的结果。如果使用Ro-31-8220抑制蛋白激酶C，则这种增强作用不会受到影响，这表明它不涉及PKC依赖性非电容性Ca（2+）进入。由CY-4引起的PAR-4激动剂AYPGKF引起的Ca（2+）输入增加到对照的133.7 +/- 12.8％，而由PAR-1激动剂SFLLRN引起的Ca（2+）信号不受影响。 。 PAR-4拮抗剂tcY-NH（2）取消了Cyt D对凝血酶诱发的Ca（2+）进入的影响。细胞表面蛋白的生物素化表明，凝血酶刺激后PAR-4被内在化。 Cyt D减少了这种内部化。这些数据表明，Cyt D阻止了PAR-4的内部化，这可能导致该受体的信号转导延长。这可能掩盖了Cyt D对PAR-4激活后SOCE激活的直接作用。

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