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Contribution of CFTR to Alveolar Fluid Clearance by Lipoxin A(4) via PI3K/Akt Pathway in LPS-Induced Acute Lung Injury
The lipoxins are the first proresolution mediators to be recognized and described as the endogenous “braking signals” for inflammation. We evaluated the anti-inflammatory and proresolution bioactions of lipoxin A(4) in our lipopolysaccharide (LPS-)induced lung injury model. We demonstrated that lipo...
Autores principales: | , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi Publishing Corporation
2013
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3671557/ https://www.ncbi.nlm.nih.gov/pubmed/23766562 http://dx.doi.org/10.1155/2013/862628 |
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author | Yang, Yi Cheng, Yang Lian, Qing-Quan Yang, Li Qi, Wei Wu, De-Rong Zheng, Xia Liu, Yong-Jian Li, Wen-Juan Jin, Sheng-Wei Smith, Fang Gao |
author_facet | Yang, Yi Cheng, Yang Lian, Qing-Quan Yang, Li Qi, Wei Wu, De-Rong Zheng, Xia Liu, Yong-Jian Li, Wen-Juan Jin, Sheng-Wei Smith, Fang Gao |
author_sort | Yang, Yi |
collection | PubMed |
description | The lipoxins are the first proresolution mediators to be recognized and described as the endogenous “braking signals” for inflammation. We evaluated the anti-inflammatory and proresolution bioactions of lipoxin A(4) in our lipopolysaccharide (LPS-)induced lung injury model. We demonstrated that lipoxin A(4) significantly improved histology of rat lungs and inhibited IL-6 and TNF-α in LPS-induced lung injury. In addition, lipoxin A(4) increased alveolar fluid clearance (AFC) and the effect of lipoxin A(4) on AFC was abolished by CFTR(inh-172) (a specific inhibitor of CFTR). Moreover, lipoxin A(4) could increase cystic fibrosis transmembrane conductance regulator (CFTR) protein expression in vitro and in vivo. In rat primary alveolar type II (ATII) cells, LPS decreased CFTR protein expression via activation of PI3K/Akt, and lipoxin A(4) suppressed LPS-stimulated phosphorylation of Akt. These results showed that lipoxin A(4) enhanced CFTR protein expression and increased AFC via PI3K/Akt pathway. Thus, lipoxin A(4) may provide a potential therapeutic approach for acute lung injury. |
format | Online Article Text |
id | pubmed-3671557 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2013 |
publisher | Hindawi Publishing Corporation |
record_format | MEDLINE/PubMed |
spelling | pubmed-36715572013-06-13 Contribution of CFTR to Alveolar Fluid Clearance by Lipoxin A(4) via PI3K/Akt Pathway in LPS-Induced Acute Lung Injury Yang, Yi Cheng, Yang Lian, Qing-Quan Yang, Li Qi, Wei Wu, De-Rong Zheng, Xia Liu, Yong-Jian Li, Wen-Juan Jin, Sheng-Wei Smith, Fang Gao Mediators Inflamm Research Article The lipoxins are the first proresolution mediators to be recognized and described as the endogenous “braking signals” for inflammation. We evaluated the anti-inflammatory and proresolution bioactions of lipoxin A(4) in our lipopolysaccharide (LPS-)induced lung injury model. We demonstrated that lipoxin A(4) significantly improved histology of rat lungs and inhibited IL-6 and TNF-α in LPS-induced lung injury. In addition, lipoxin A(4) increased alveolar fluid clearance (AFC) and the effect of lipoxin A(4) on AFC was abolished by CFTR(inh-172) (a specific inhibitor of CFTR). Moreover, lipoxin A(4) could increase cystic fibrosis transmembrane conductance regulator (CFTR) protein expression in vitro and in vivo. In rat primary alveolar type II (ATII) cells, LPS decreased CFTR protein expression via activation of PI3K/Akt, and lipoxin A(4) suppressed LPS-stimulated phosphorylation of Akt. These results showed that lipoxin A(4) enhanced CFTR protein expression and increased AFC via PI3K/Akt pathway. Thus, lipoxin A(4) may provide a potential therapeutic approach for acute lung injury. Hindawi Publishing Corporation 2013 2013-05-16 /pmc/articles/PMC3671557/ /pubmed/23766562 http://dx.doi.org/10.1155/2013/862628 Text en Copyright © 2013 Yi Yang et al. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Article Yang, Yi Cheng, Yang Lian, Qing-Quan Yang, Li Qi, Wei Wu, De-Rong Zheng, Xia Liu, Yong-Jian Li, Wen-Juan Jin, Sheng-Wei Smith, Fang Gao Contribution of CFTR to Alveolar Fluid Clearance by Lipoxin A(4) via PI3K/Akt Pathway in LPS-Induced Acute Lung Injury |
title | Contribution of CFTR to Alveolar Fluid Clearance by Lipoxin A(4) via PI3K/Akt Pathway in LPS-Induced Acute Lung Injury |
title_full | Contribution of CFTR to Alveolar Fluid Clearance by Lipoxin A(4) via PI3K/Akt Pathway in LPS-Induced Acute Lung Injury |
title_fullStr | Contribution of CFTR to Alveolar Fluid Clearance by Lipoxin A(4) via PI3K/Akt Pathway in LPS-Induced Acute Lung Injury |
title_full_unstemmed | Contribution of CFTR to Alveolar Fluid Clearance by Lipoxin A(4) via PI3K/Akt Pathway in LPS-Induced Acute Lung Injury |
title_short | Contribution of CFTR to Alveolar Fluid Clearance by Lipoxin A(4) via PI3K/Akt Pathway in LPS-Induced Acute Lung Injury |
title_sort | contribution of cftr to alveolar fluid clearance by lipoxin a(4) via pi3k/akt pathway in lps-induced acute lung injury |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3671557/ https://www.ncbi.nlm.nih.gov/pubmed/23766562 http://dx.doi.org/10.1155/2013/862628 |
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