ENaCs as Both Effectors and Regulators of MiRNAs in Lung Epithelial Development and Regeneration.
ENaCs as Both Effectors and Regulators of MiRNAs in Lung Epithelial Development and Regeneration.
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ENaC 在肺上皮发育和再生中作为 miRNA 的效应器和调节器
DOI：
10.1159/000485417
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发表时间：
2017
期刊：
影响因子：
--
通讯作者：
Ji HL
中科院分区：
文献类型：
--
作者：
Ding Y;Zhao R;Zhao X;Matthay MA;Nie HG;Ji HL
上皮钠通道（ENaC）通过在气道、肺、肾和结肠的致密上皮上建立渗透性Na+梯度，在重新吸收过多的腔液中起重要作用。ENaC也是盐在肾脏中潴留的主要途径。MicroRNAs （miRs）是一组在转录后水平调控基因表达的非编码rna，已成为ENaC的一类新型调控因子。鉴于ENaC通路对于维持肺、肾和其他腔体的体液稳态至关重要，我们总结了ENaC和mir之间的串导，并概述了潜在的调节因子，包括肺和其他上皮组织/器官中的醛固酮、转化生长因子-β1和血管内皮生长因子- a。我们比较了正常小鼠和受伤小鼠和人肺的miRs谱，发现LPS和呼吸机诱导的ARDS小鼠模型中许多miRs发生了显著变化。此外，我们重申了miRs对ENaC在基于干细胞/祖细胞的再上皮化中的潜在调节作用，并确定了ENaC的一个有希望的药物靶点，即通过间充质干细胞释放的旁分泌去除ARDS中的水肿液。综上所述，miRs和scn1s /ENaCs之间的相互作用似乎对肺发育、成人肺上皮细胞更新和再上皮化修复至关重要。
Epithelial sodium channels (ENaC) play an important role in re-absorbing excessive luminal fluid by building up an osmotic Na+ gradient across the tight epithelium in the airway, the lung, the kidney, and the colon. The ENaC is a major pathway for retention of salt in kidney too. MicroRNAs (miRs), a group of non-coding RNAs that regulate gene expression at the post-transcriptional level, have emerged as a novel class of regulators for ENaC. Given the ENaC pathway is crucial for maintaining fluid homeostasis in the lung and the kidney and other cavities, we summarized the cross-talk between ENaC and miRs and recapitulated the underlying regulatory factors, including aldosterone, transforming growth factor-β1, and vascular endothelial growth factor-A in the lung and other epithelial tissues/organs. We have compared the profiling of miRs between normal and injured mice and human lungs, which showed a significant alteration in numerous miRs in mouse models of LPS and ventilator induced ARDS. In addition, we reiterated the potential regulation of the ENaC by miRs in stem/ progenitor cell-based re-epithelialization, and identified a promising pharmaceutic target of ENaC for removing edema fluid in ARDS by mesenchymal stem cells-released paracrine. In conclusion, it seems that the interactions between miRs and scnn1s/ENaCs are critical for lung development, epithelial cell turnover in adult lungs, and re-epithelialization for repair.
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