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

August-2014 Volume 10 Issue 2

Full Size Image

Journals

International Journal of Molecular Medicine

International Journal of Molecular Medicine is an international journal devoted to molecular mechanisms of human disease.

International Journal of Oncology

International Journal of Oncology is an international journal devoted to oncology research and cancer treatment.

Molecular Medicine Reports

Covers molecular medicine topics such as pharmacology, pathology, genetics, neuroscience, infectious diseases, molecular cardiology, and molecular surgery.

Oncology Reports

Oncology Reports is an international journal devoted to fundamental and applied research in Oncology.

Experimental and Therapeutic Medicine

Experimental and Therapeutic Medicine is an international journal devoted to laboratory and clinical medicine.

Oncology Letters

Oncology Letters is an international journal devoted to Experimental and Clinical Oncology.

Biomedical Reports

Explores a wide range of biological and medical fields, including pharmacology, genetics, microbiology, neuroscience, and molecular cardiology.

Molecular and Clinical Oncology

International journal addressing all aspects of oncology research, from tumorigenesis and oncogenes to chemotherapy and metastasis.

World Academy of Sciences Journal

Multidisciplinary open-access journal spanning biochemistry, genetics, neuroscience, environmental health, and synthetic biology.

International Journal of Functional Nutrition

Open-access journal combining biochemistry, pharmacology, immunology, and genetics to advance health through functional nutrition.

International Journal of Epigenetics

Publishes open-access research on using epigenetics to advance understanding and treatment of human disease.

Medicine International

An International Open Access Journal Devoted to General Medicine.

August-2014 Volume 10 Issue 2

Full Size Image

Article

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
View Affiliations / Copyright

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
Pages: 773-777
|
Published online on: June 6, 2014

https://doi.org/10.3892/mmr.2014.2303
Expand metrics +

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.

View Figures

View References

1	Maybauer MO, Maybauer DM and Herndon DN: Incidence and outcomes of acute lung injury. N Engl J Med. 354:416–417. 2006. View Article : Google Scholar : PubMed/NCBI
2	Ware LB and Matthay MA: Alveolar fluid clearance is impaired in the majority of patients with acute lung injury and the acute respiratory distress syndrome. Am J Respir Crit Care Med. 163:1376–1383. 2001. View Article : Google Scholar : PubMed/NCBI
3	Berthiaume Y, Folkesson HG and Matthay MA: Lung edema clearance: 20 years of progress: invited review: alveolar edema fluid clearance in the injured lung. J Appl Physiol (1985). 93:2207–2213. 2002.PubMed/NCBI
4	Canessa CM, Schild L, Buell G, et al: Amiloride-sensitive epithelial Na⁺ channel is made of three homologous subunits. Nature. 367:463–467. 1994. View Article : Google Scholar : PubMed/NCBI
5	Hummler E, Barker P, Gatzy J, et al: Early death due to defective neonatal lung liquid clearance in alpha-ENaC-deficient mice. Nat Genet. 12:325–328. 1996. View Article : Google Scholar : PubMed/NCBI
6	Egli M, Duplain H, Lepori M, et al: Defective respiratory amiloride-sensitive sodium transport predisposes to pulmonary oedema and delays its resolution in mice. J Physiol. 560:857–865. 2004. View Article : Google Scholar : PubMed/NCBI
7	Rittirsch D, Flierl MA, Day DE, et al: Acute lung injury induced by lipopolysaccharide is independent of complement activation. J Immunol. 180:7664–7672. 2008. View Article : Google Scholar : PubMed/NCBI
8	Dagenais A, Gosselin D, Guilbault C, et al: Modulation of epithelial sodium channel (ENaC) expression in mouse lung infected with Pseudomonas aeruginosa. Respir Res. 6:22005. View Article : Google Scholar : PubMed/NCBI
9	Dodrill MW and Fedan JS: Lipopolysaccharide hyperpolarizes guinea pig airway epithelium by increasing the activities of the epithelial Na(+) channel and the Na(+)-K(+) pump. Am J Physiol Lung Cell Mol Physiol. 299:L550–L558. 2010. View Article : Google Scholar : PubMed/NCBI
10	Baines DL, Albert AP, Hazell MJ, et al: Lipopolysaccharide modifies amiloride-sensitive Na⁺ transport processes across human airway cells: role of mitogen-activated protein kinases ERK 1/2 and 5. Pflugers Arch. 459:451–463. 2010.PubMed/NCBI
11	Song JJ, Kwon SK, Cho CG, et al: Expression of ENaC in LPS-induced inflammation of middle ear mucosa. Acta Otolaryngol. 132:1145–1150. 2012. View Article : Google Scholar : PubMed/NCBI
12	Dodrill MW, Beezhold DH, Meighan T, et al: Lipopolysaccharide increases Na(+), K(+)-pump, but not ENaC, expression in guinea-pig airway epithelium. Eur J Pharmacol. 651:176–186. 2011. View Article : Google Scholar : PubMed/NCBI
13	Su X, Wang L, Song Y and Bai C: Inhibition of inflammatory responses by ambroxol, a mucolytic agent, in a murine model of acute lung injury induced by lipopolysaccharide. Intensive Care Med. 30:133–140. 2003. View Article : Google Scholar : PubMed/NCBI
14	Berthiaume Y and Matthay MA: Alveolar edema fluid clearance and acute lung injury. Respir Physiol Neurobiol. 159:350–359. 2007. View Article : Google Scholar : PubMed/NCBI
15	Roux J, Kawakatsu H, Gartland B, et al: Interleukin-1beta decreases expression of the epithelial sodium channel alpha-subunit in alveolar epithelial cells via a p38 MAPK-dependent signaling pathway. J Biol Chem. 280:18579–18589. 2005. View Article : Google Scholar : PubMed/NCBI
16	Galietta LJ, Pagesy P, Folli C, et al: IL-4 is a potent modulator of ion transport in the human bronchial epithelium in vitro. J Immunol. 168:839–845. 2002. View Article : Google Scholar : PubMed/NCBI
17	Galietta LJ, Folli C, Marchetti C, et al: Modification of transepithelial ion transport in human cultured bronchial epithelial cells by interferon-gamma. Am J Physiol Lung Cell Mol Physiol. 278:L1186–L1194. 2000.PubMed/NCBI
18	Frank J, Roux J, Kawakatsu H, et al: Transforming growth factor-beta1 decreases expression of the epithelial sodium channel alphaENaC and alveolar epithelial vectorial sodium and fluid transport via an ERK1/2-dependent mechanism. J Biol Chem. 278:43939–43950. 2003. View Article : Google Scholar
19	Clerici C and Matthay MA: Hypoxia regulates gene expression of alveolar epithelial transport proteins. J Appl Physiol (1985). 88:1890–1896. 2000.PubMed/NCBI
20	Wodopia R, Ko HS, Billian J, et al: Hypoxia decreases proteins involved in epithelial electrolyte transport in A549 cells and rat lung. Am J Physiol Lung Cell Mol Physiol. 279:L1110–L1119. 2000.PubMed/NCBI
21	Rezaiguia S, Garat C, Delclaux C, et al: Acute bacterial pneumonia in rats increases alveolar epithelial fluid clearance by a tumor necrosis factor-alpha-dependent mechanism. J Clin Invest. 99:325–335. 1997. View Article : Google Scholar
22	Viget NB, Guery BP, Ader F, et al: Keratinocyte growth factor protects against Pseudomonas aeruginosa-induced lung injury. Am J Physiol Lung Cell Mol Physiol. 279:1199–1209. 2000.

Journals

International Journal of Molecular Medicine

International Journal of Oncology

Molecular Medicine Reports

Oncology Reports

Experimental and Therapeutic Medicine

Oncology Letters

Biomedical Reports

Molecular and Clinical Oncology

World Academy of Sciences Journal

International Journal of Functional Nutrition

International Journal of Epigenetics

Medicine International

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

This article is mentioned in:

Abstract

Figure 1

Figure 2

Figure 3

Figure 4

Related Articles