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首页> 外文期刊>American Journal of Physiology >In vitro and in vivo regulation of transepithelial lung alveolar sodium transport by serine proteases.
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In vitro and in vivo regulation of transepithelial lung alveolar sodium transport by serine proteases.

机译：丝氨酸蛋白酶对上皮肺肺泡钠运输的体内和体外调节。

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摘要

The amiloride-sensitive epithelial sodium channel (ENaC) constitutes a rate-limiting step for sodium (Na+) and water absorption across lung alveolar epithelium. Recent reports suggested that ENaC is regulated by membrane-bound extracellular serine proteases, such as channel-activating proteases (CAPs). The objectives of this study were to examine the role of serine proteases in the regulation of transepithelial alveolar Na+ and water transport in vitro and in vivo and the expression of CAPs in rodent distal lung. In vitro experiments showed that inhibition of endogenous serine proteases by apical aprotinin 1) decreased ENaC-mediated currents in primary cultures of rat and mouse alveolar epithelial cells without affecting the abundance nor the electrophoretic migration pattern of biotinylated alpha- and beta-ENaC expressed at the cell surface and 2) suppressed the increase in amiloride-sensitive short-circuit current induced by the beta2-agonist terbutaline. RT-PCR experiments indicated that CAP1, CAP2,and CAP3 mRNAs were expressed in mouse alveolar epithelial cells, whereas CAP1 was also expressed in alveolar macrophages recovered by bronchoalveolar lavage. CAP1 protein was detected by Western blotting in rat and mouse alveolar epithelial cells, alveolar macrophages and bronchoalveolar lavage fluid. Finally, in vivo experiments revealed that intra-alveolar treatment with aprotinin abolished the increase in Na+-driven alveolar fluid clearance (AFC) induced by terbutaline in an in situ mouse lung model, whereas trypsin potentiated it. These results show that endogenous membrane-bound and/or secreted serine proteases such as CAPs regulate alveolar Na+ and fluid transport in vitro and in vivo in rodent lung.
机译：阿米洛利敏感的上皮钠通道（ENaC）构成了跨肺泡上皮的钠（Na +）和吸水率的限速步骤。最近的报道表明，ENaC受膜结合的细胞外丝氨酸蛋白酶（例如通道激活蛋白酶（CAPs））的调节。这项研究的目的是检查丝氨酸蛋白酶在调节上皮肺泡Na +和体内和体外水运输中的作用以及在啮齿动物远端肺中CAPs的表达。体外实验表明，顶端抑肽酶对内源性丝氨酸蛋白酶的抑制作用1）降低了大鼠和小鼠肺泡上皮细胞原代培养物中ENaC介导的电流，而不影响在该处表达的生物素化的α-和β-ENaC的丰度或电泳迁移模式。细胞表面和2）抑制了由β2-激动剂特布他林引起的对阿米洛利敏感的短路电流的增加。 RT-PCR实验表明，CAP1，CAP2和CAP3 mRNA在小鼠肺泡上皮细胞中表达，而CAP1在肺泡巨噬细胞中被支气管肺泡灌洗所表达。通过蛋白质印迹法在大鼠和小鼠的肺泡上皮细胞，肺泡巨噬细胞和支气管肺泡灌洗液中检测到CAP1蛋白。最后，体内实验表明，在原位小鼠肺模型中，用抑肽酶进行的肺泡内治疗消除了特布他林诱导的Na +驱动的肺泡液清除率（AFC）的增加，而胰蛋白酶增强了这种作用。这些结果表明，内源性膜结合和/或分泌的丝氨酸蛋白酶（如CAPs）在啮齿动物肺中体外和体内调节肺泡Na +和液体运输。

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