Biphasic modulation of α-ENaC expression by lipopolysaccharide in vitro and in vivo

Sheng,Shu-Jing; Nie,Yi-Chu; Lin,Feng; Li,Pei-Bo; Liu,Meng‑Hua; Xie,Cheng-Shi; Long,Chao-Feng; Su,Wei-Wei

doi:10.3892/mmr.2014.2303

Biphasic modulation of α-ENaC expression by lipopolysaccharide in vitro and in vivo

Authors:
- Shu-Jing Sheng
- Yi-Chu Nie
- Feng Lin
- Pei-Bo Li
- Meng‑Hua Liu
- Cheng-Shi Xie
- Chao-Feng Long
- Wei-Wei Su
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Affiliations: Guangzhou Quality R&D Center of Traditional Chinese Medicine, Guangdong Key Laboratory of Plant Resources, School of Life Sciences, Sun Yat-Sen University, Guangzhou, Guangdong 510275, P.R. China, Guangdong Zhongsheng Pharmaceutical Co., Ltd., Dongguan, Guangdong 523325, P.R. China
Published online on: June 6, 2014 https://doi.org/10.3892/mmr.2014.2303
Pages: 773-777

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Abstract

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.

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