Abstract |
Reduced alveolar fluid clearance (AFC) is a major pathological feature of acute lung injury (ALI). Epithelial sodium channel (ENaC) plays a key role in regulating the transport of Na+ and clearing alveolar edema fluid effectively. ENaC has been reported to be regulated by aldosterone in the distal collecting tube of the kidney. We hypothesized whether aldosterone regulated ENaC in alveolar epithelium and correspondingly played a role in ALI. In this study we found that the expression of aldosterone synthesis encoding gene, CYP11B2, and ENaC were decreased in the lung tissue of LPS-induced ALI mice. Furthermore, aldosterone alleviated ALI by increasing the expression of ENaC-α and relieving pulmonary edema. Besides, we found that aldosterone upregulated ENaC-α through PI3K/Akt/SGK1 pathway. In conclusion, our study demonstrated that aldosterone attenuated pulmonary edema by upregulating ENaC-α through the PI3K/Akt/SGK1 pathway in LPS-induced ALI, indicating that aldosterone might be a promising adjuvant drug for ALI treatment.
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Authors | Xiu Fei, Yu Ziqian, Yang Bingwu, Li Min, Xian Xinmiao, Meng Zhen, Guo Lirong, Wang Song |
Journal | Molecular and cellular probes
(Mol Cell Probes)
Vol. 57
Pg. 101709
(06 2021)
ISSN: 1096-1194 [Electronic] England |
PMID | 33713776
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Copyright | Copyright © 2021 Elsevier Ltd. All rights reserved. |
Chemical References |
- Epithelial Sodium Channels
- Lipopolysaccharides
- Aldosterone
- Proto-Oncogene Proteins c-akt
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Topics |
- Acute Lung Injury
(chemically induced, drug therapy)
- Aldosterone
- Animals
- Epithelial Sodium Channels
(genetics, metabolism)
- Lipopolysaccharides
- Mice
- Phosphatidylinositol 3-Kinases
(metabolism)
- Proto-Oncogene Proteins c-akt
(metabolism)
- Signal Transduction
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