ENaCs as Both Effectors and Regulators of MiRNAs in Lung Epithelial Development and Regeneration
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...
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| Format: | Article |
| Language: | English |
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Cell Physiol Biochem Press GmbH & Co KG
2017-11-01
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| Series: | Cellular Physiology and Biochemistry |
| Subjects: | |
| Online Access: | https://www.karger.com/Article/FullText/485417 |
| _version_ | 1818863598236073984 |
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| author | Yan Ding Runzhen Zhao Xiaoli Zhao Michael A. Matthay Hong-Guang Nie Hong-Long Ji |
| author_facet | Yan Ding Runzhen Zhao Xiaoli Zhao Michael A. Matthay Hong-Guang Nie Hong-Long Ji |
| author_sort | Yan Ding |
| collection | DOAJ |
| description | 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. |
| first_indexed | 2024-12-19T10:18:18Z |
| format | Article |
| id | doaj.art-7efdad14e4bc4b4eb4563ef29495e984 |
| institution | Directory Open Access Journal |
| issn | 1015-8987 1421-9778 |
| language | English |
| last_indexed | 2024-12-19T10:18:18Z |
| publishDate | 2017-11-01 |
| publisher | Cell Physiol Biochem Press GmbH & Co KG |
| record_format | Article |
| series | Cellular Physiology and Biochemistry |
| spelling | doaj.art-7efdad14e4bc4b4eb4563ef29495e9842022-12-21T20:26:08ZengCell Physiol Biochem Press GmbH & Co KGCellular Physiology and Biochemistry1015-89871421-97782017-11-014431120113210.1159/000485417485417ENaCs as Both Effectors and Regulators of MiRNAs in Lung Epithelial Development and RegenerationYan DingRunzhen ZhaoXiaoli ZhaoMichael A. MatthayHong-Guang NieHong-Long JiEpithelial 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.https://www.karger.com/Article/FullText/485417Epithelial reparationStem/progenitor cellsRe-epithelializationNon-coding RNATransepithelial sodium transportCross talkAmiloride-sensitive sodium channels |
| spellingShingle | Yan Ding Runzhen Zhao Xiaoli Zhao Michael A. Matthay Hong-Guang Nie Hong-Long Ji ENaCs as Both Effectors and Regulators of MiRNAs in Lung Epithelial Development and Regeneration Cellular Physiology and Biochemistry Epithelial reparation Stem/progenitor cells Re-epithelialization Non-coding RNA Transepithelial sodium transport Cross talk Amiloride-sensitive sodium channels |
| title | ENaCs as Both Effectors and Regulators of MiRNAs in Lung Epithelial Development and Regeneration |
| title_full | ENaCs as Both Effectors and Regulators of MiRNAs in Lung Epithelial Development and Regeneration |
| title_fullStr | ENaCs as Both Effectors and Regulators of MiRNAs in Lung Epithelial Development and Regeneration |
| title_full_unstemmed | ENaCs as Both Effectors and Regulators of MiRNAs in Lung Epithelial Development and Regeneration |
| title_short | ENaCs as Both Effectors and Regulators of MiRNAs in Lung Epithelial Development and Regeneration |
| title_sort | enacs as both effectors and regulators of mirnas in lung epithelial development and regeneration |
| topic | Epithelial reparation Stem/progenitor cells Re-epithelialization Non-coding RNA Transepithelial sodium transport Cross talk Amiloride-sensitive sodium channels |
| url | https://www.karger.com/Article/FullText/485417 |
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