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首页> 外文期刊>Platelets >Effect of neutrophil adhesion on the size of aggregates formed by agonist-activated platelets.
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Effect of neutrophil adhesion on the size of aggregates formed by agonist-activated platelets.

机译：中性粒细胞粘附对激动剂激活的血小板形成的聚集体大小的影响。

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In this study we have investigated the effect of human neutrophil on agonist-induced platelet aggregation by using the laser-light scattering method that can detect a two-phase process, formation of small aggregates followed by large aggregate formation. When nonstimulated neutrophils were added to agonist-stimulated platelet-rich plasma (PRP), the large platelet aggregates were decreased and the small ones were increased by using either collagen, thrombin or ADP as agonist. Scanning-electron microscopic observation showed marked adhesion of neutrophil to aggregated platelets. The supernatant from neutrophils cell lysate (neutrophil supernatant) showed inhibitory effect similar to that with intact neutrophils, suggesting that the inhibitory effect by neutrophils was due to soluble component(s) including proteases released from neutrophils adhered to activated platelets. We have examined the effect of inhibition of a major released protease, elastase. The addition of its potent inhibitor elafin to intact neutrophils or the neutrophil supernatant changed their antiaggregating activity. The treatment of platelets with genistein, an inhibitor of protein tyrosine kinase, decreased agonist-induced large aggregates and increased small ones, suggesting that certain protein tyrosine kinase would be involved in the transition from small to large platelet aggregates. It was also shown that the tyrosine phosphorylation induced by agonist stimulation of several high molecular-weight proteins of platelets was inhibited by coincubation with neutrophils, concurrent with increases in smaller phosphorylated proteins. In washed platelets, coincubation with neutrophils resulted in reduced formation of large aggregates when stimulated with collagen or thrombin and repressed agonist-induced activation of tyrosine protein kinases (Syk, Lyn, Src, and Pyk2), but not thrombin-induced ERK and p38 MAP kinase. These results suggest that the cleavage of platelet membrane glycoproteins at least in part by elastase which was released from neutrophils, is involved in the inhibition of the transition from small to large platelet aggregates.
机译：在这项研究中，我们使用激光散射法研究了人类嗜中性粒细胞对激动剂诱导的血小板聚集的影响，该方法可以检测到两个阶段的过程：先形成小聚集体，然后形成大聚集体。当将非刺激性嗜中性粒细胞添加到激动剂刺激的富含血小板的血浆（PRP）中时，使用胶原蛋白，凝血酶或ADP作为激动剂可以减少大的血小板聚集物，而增加小的血小板聚集物。扫描电子显微镜观察显示嗜中性粒细胞明显粘附于聚集的血小板。中性粒细胞裂解液的上清液（中性粒细胞上清液）显示出与完整中性粒细胞相似的抑制作用，表明中性粒细胞的抑制作用是由于可溶性成分（包括从中性粒细胞释放的蛋白酶）粘附在活化的血小板上。我们已经检查了抑制主要释放的蛋白酶弹性蛋白酶的作用。在完整的嗜中性粒细胞或嗜中性粒细胞上清液中加入其有效抑制剂抑素可改变其抗聚集活性。金雀异黄素（一种蛋白酪氨酸激酶的抑制剂）对血小板的处理减少了激动剂诱导的大聚集物，而增加了小聚集物，表明某些蛋白酪氨酸激酶将参与从小到大的血小板聚集物的转变。还显示通过与嗜中性粒细胞共孵育抑制了激动剂刺激血小板的几种高分子量蛋白质诱导的酪氨酸磷酸化，同时增加了较小的磷酸化蛋白质。在洗涤过的血小板中，与中性粒细胞共孵育可在胶原蛋白或凝血酶刺激下减少大聚集体的形成，并抑制激动剂诱导的酪氨酸蛋白激酶（Syk，Lyn，Src和Pyk2）的活化，但不能抑制凝血酶诱导的ERK和p38 MAP激酶。这些结果表明，从嗜中性粒细胞释放的弹性蛋白酶对血小板膜糖蛋白的切割至少部分地参与了从小血小板聚集物向大血小板聚集物的转变的抑制。

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