Biphasic modulation of α-ENaC expression by lipopolysaccharide in vitro and in vivo
| Autor: | Shujing Sheng, Weiwei Su, Feng Lin, Yi-Chu Nie, Meng‑Hua Liu, Cheng-Shi Xie, Peibo Li, Chao-feng Long |
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| Rok vydání: | 2014 |
| Předmět: |
Lipopolysaccharides
Male inorganic chemicals Epithelial sodium channel Cancer Research Time Factors Lipopolysaccharide Acute Lung Injury Inflammation Pharmacology Lung injury Biology Biochemistry Pathogenesis Mice chemistry.chemical_compound In vivo Cell Line Tumor Genetics medicine Animals Humans RNA Messenger Epithelial Sodium Channels Lung Molecular Biology urogenital system respiratory system Hypoxia (medical) Pulmonary edema medicine.disease Immunohistochemistry respiratory tract diseases Oncology chemistry Cancer research Molecular Medicine Female medicine.symptom hormones hormone substitutes and hormone antagonists |
| Zdroj: | Molecular Medicine Reports. 10:773-777 |
| ISSN: | 1791-3004 1791-2997 |
| DOI: | 10.3892/mmr.2014.2303 |
| Popis: | Acute lung injury (ALI) is characterized by pulmonary edema, in which the epithelial sodium channel (ENaC) has a critical role in the clearance of edema fluid from the alveolar space. Lipopolysaccharide (LPS), frequently employed to induce ALI in experimental animal models, has been reported to regulate ENaC expression and alveolar fluid clearance. The role of LPS in regulating ENaC expression is currently controversial, with increases and decreases reported in ENaC expression in response to LPS treatment, as well as reports that ENaC expression is not affected by LPS induction. The present study aimed to systematically analyze the regulation of α‑ENaC expression in LPS models of ALI at different pathological stages in vitro and in vivo. ENaC expression was observed to increase ≤8 h after LPS treatment, and to decrease thereafter. This finding may explain the contradictory data regarding α‑ENaC expression in response to LPS in the lung. The results of the present study, in combination with those of previous studies, indicate that the modulation of α-ENaC expression may not be a direct genetic response to LPS exposure, but a general response of the lung to the pathological changes associated with inflammation, hypoxia and endothelial and epithelial damage involved in the development of ALI. The findings of this study may have potential clinical significance for understanding the pathogenesis of ALI and improving patient outcome. |
| Databáze: | OpenAIRE |
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