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首页> 美国卫生研究院文献>American Journal of Physiology - Lung Cellular and Molecular Physiology >Platelets induce endothelial tissue factor expression in a mouse model of acid-induced lung injury
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Platelets induce endothelial tissue factor expression in a mouse model of acid-induced lung injury

机译：血小板在酸性肺损伤小鼠模型中诱导内皮组织因子表达

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Although the lung expresses procoagulant proteins under inflammatory conditions, underlying mechanisms remain unclear. Here, we addressed lung endothelial expression of tissue factor (TF), which initiates the coagulation cascade and expression of which signifies development of a procoagulant phenotype in the vasculature. To establish the model of acid-induced acute lung injury (ALI), we intranasally instilled anesthetized mice with saline or acid. Then 2 h later, we isolated pulmonary vascular cells for flow cytometry and confocal microscopy to detect the leukocyte antigen, CD45 and the endothelial markers VE-cadherin and von Willebrand factor (vWf). Acid increased both the number of vWf-expressing cells as well as TF and P-selectin expressions on these cells. All of these effects were markedly inhibited by treating mice with antiplatelet serum, suggesting the involvement of platelets. The increased expressions of TF, vWf, and P-selectin in response to acid also occurred in platelets. Moreover, the effects were replicated in endothelial cells derived from isolated, blood-perfused lungs. However, the effect was inhibited completely in lungs perfused with platelet-depleted and, to a lesser extent, with leukocyte-depleted blood. Acid injury increased endothelial expressions of the platelet proteins, CD41 and CD42b, providing evidence that platelet proteins were transferred to the vascular surface. Reactive oxygen species (ROS) were implicated in these responses, in that the endothelial and platelet protein expressions were inhibited. We conclude that acid-induced ALI causes NOX2-mediated ROS generation that activates platelets, which then generate a procoagulant endothelial surface.
机译：尽管肺在炎症条件下表达促凝蛋白，但其潜在机制仍不清楚。在这里，我们解决了组织因子（TF）的肺内皮表达，它启动了凝血级联反应，其表达表明了脉管系统中促凝表型的发展。为了建立酸诱导的急性肺损伤（ALI）模型，我们用盐水或酸滴鼻麻醉了小鼠。然后2小时后，我们分离了肺血管细胞进行流式细胞术和共聚焦显微镜检查，以检测白细胞抗原，CD45以及内皮标志物VE-cadherin和von Willebrand因子（vWf）。酸增加了表达vWf的细胞的数量以及这些细胞上TF和P选择素的表达。通过用抗血小板血清治疗小鼠，所有这些作用均被显着抑制，表明血小板参与其中。血小板中也发生了TF，vWf和P-选择素表达对酸的反应。此外，这种作用在源自分离的血液灌注肺的内皮细胞中得以复制。但是，在灌注了贫血小板的肺以及灌注了白血球的血液后，这种作用在肺中被完全抑制了。酸损伤增加了血小板蛋白CD41和CD42b的内皮表达，这提供了血小板蛋白已转移到血管表面的证据。活性氧（ROS）参与这些反应，因为内皮和血小板蛋白的表达受到抑制。我们得出的结论是，酸诱导的ALI会引起NOX2介导的ROS生成，从而激活血小板，然后生成促凝内皮表面。

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