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首页> 外文期刊>Cellular Physiology and Biochemistry >P63 (CKAP4) as an SP-A Receptor: Implications for Surfactant Turnover
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P63 (CKAP4) as an SP-A Receptor: Implications for Surfactant Turnover

机译：P63（CKAP4）作为SP-A受体：对表面活性剂周转的影响

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Surfactant protein-A (SP-A) plays an important role in the clearance of surfactant from the lung alveolar space and in the regulation of surfactant secretion and uptake by type II pneumocytes in culture. Two pathways are important for the endocytosis of surfactant by type II cells and the intact lung, a receptor-mediated clathrin-dependent pathway and a non-clathrin, actin-mediated pathway. The critical role of the clathrin/receptor-mediated pathway in normal mice is supported by the finding that SP-A gene-targeted mice use the actin-dependent pathway to maintain normal clearance of surfactant. Addition of SP-A to the surfactant of the SP-A null mice “rescued” the phenotype, further emphasizing the essential role of the SP-A/receptor-mediated process in surfactant turnover. This review presents an overview of the structure of SP-A and its function in surfactant turnover. The evidence that the interaction of SP-A with type II cells is a receptor-mediated process is presented. A newly identified receptor for SP-A, P63/CKAP4, is described in detail, with elucidation of the specific structural features of this 63 kDa, nonglycosylated, highly coiled, transmembrane protein. The compelling evidence that P63 functions as a receptor for SP-A on type II cells is summarized. Regulation of P63 receptor density on the surface of pneumocytes may be a novel approach for the regulation of surfactant homeostasis by the lung.
机译：表面活性剂蛋白A（SP-A）在从肺泡间隙清除表面活性剂以及调节培养物中II型肺细胞的表面活性剂分泌和摄取方面起着重要作用。对于II型细胞和完整的肺内表面活性剂的内吞作用，两个途径很重要，即受体介导的网格蛋白依赖性途径和非clathrin的肌动蛋白介导途径。网格蛋白/受体介导的途径在正常小鼠中的关键作用得到了以下发现的支持：以SP-A基因为靶点的小鼠使用肌动蛋白依赖性途径维持表面活性剂的正常清除。将SP-A添加到SP-A无效小鼠的表面活性剂中“挽救”了表型，进一步强调了SP-A /受体介导的过程在表面活性剂更新过程中的重要作用。这篇综述概述了SP-A的结构及其在表面活性剂更新中的功能。提出了SP-A与II型细胞相互作用是受体介导的过程的证据。详细介绍了新鉴定的SP-A受体P63 / CKAP4，并阐明了这种63 kDa非糖基化，高度卷曲的跨膜蛋白的特定结构特征。总结了P63充当II型细胞上SP-A受体的有力证据。调节肺细胞表面P63受体的密度可能是通过肺调节表面活性剂稳态的一种新方法。

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