Molecular regulation of ENaC in the process of recovery in permeability lung edema

肺泡上皮细胞具有向细胞内转运钠离子的能力。在正常情况下，这种机制允许肺泡空间保持干燥，并可以保护肺泡和毛细血管之间的屏障。我们证实，在高氧诱导的肺损伤中，上皮细胞钠通道(ENaC)不仅在数量上减少，而且在功能上减少。此外，糖皮质激素治疗上调了基因和蛋白的表达，并通过ENaC促进了肺泡液的清除。在正常情况下，ENaC与水从肺泡空间输送到肺泡上皮细胞并维持无液体状态有关。在急性肺损伤模型中，ENaC被内毒素、促炎细胞因子下调，氧化应激抑制糖皮质激素依赖的ENaC转录。认为基因表达和蛋白表达减少是急性肺损伤发生的重要原因。然而，ENaC在通透性肺水肿恢复中的作用从未被研究过。在这一点上，研究是原创的，也是独一无二的。

Alveolar epithelial cells have the ability of transporting sodium ion into cells. Under normal conditions, that mechanism allows alveolar space to keep dry, and can protect the barrier between alveoli and capillaries. We confirmed that in hyperoxia-induced lung injury epithelia sodium channel (ENaC) was reduced not just in quantity but in function. In addition to that, gene and protein expression were upregulated by the treatment of glucocorticoidm, and the removal of alveolar fluid progressed via ENaC. Under normal condition, ENaC relates to the transport of water from alveolar spce into alveolar epithelia cells and maintain fluid-free state. It reports in the model of acute lung injury that ENaC is downregulated by endotoxin, proinflammatory cytokines, and that oxidative stress inhibits the glucocorticoid dependent transcription of ENaC. It is thought that reduction of gene expression and protein expression is the important role to play in the onset of acute lung injury. However, it has never been investigated the point ENaC in recovery from permeability lung edema. In this point, the research is original, and unique.