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Nogo-B protects mice against lipopolysaccharide-induced acute lung injury
Nogo-B, a member of the reticulon 4 protein family, plays a critical role in tissue repair and acute inflammation. Its role in acute lung injury (ALI) remains unclear. Here, we assessed the function of Nogo-B during tissue injury in a lipopolysaccharide (LPS)-induced ALI mouse model. We found that p...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4502524/ https://www.ncbi.nlm.nih.gov/pubmed/26174362 http://dx.doi.org/10.1038/srep12061 |
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author | Xu, Wujian Zhu, Ying Ning, Yunye Dong, Yuchao Huang, Haidong Zhang, Wei Sun, Qinying Li, Qiang |
author_facet | Xu, Wujian Zhu, Ying Ning, Yunye Dong, Yuchao Huang, Haidong Zhang, Wei Sun, Qinying Li, Qiang |
author_sort | Xu, Wujian |
collection | PubMed |
description | Nogo-B, a member of the reticulon 4 protein family, plays a critical role in tissue repair and acute inflammation. Its role in acute lung injury (ALI) remains unclear. Here, we assessed the function of Nogo-B during tissue injury in a lipopolysaccharide (LPS)-induced ALI mouse model. We found that pulmonary Nogo-B was significantly repressed after LPS instillation in C57BL/6 mice. Over-expression of pulmonary Nogo-B using an adenovirus vector carrying the Nogo-B-RFP-3flag gene (Ad-Nogo-B) significantly prolonged the survival of mice challenged with a lethal dose of LPS. The Ad-Nogo-B-treated mice also had less severe lung injury, less alveolar protein exudation, and a higher number of macrophages but less neutrophil infiltration compared with Ad-RFP-treated mice. Interestingly, microarray analysis showed that the Ad-Nogo-B-treated mice had different gene expression profiles compared with the controls and the prominent expression of genes related to wound healing and the humoral immune response after LPS induction. Of the 49 differently expressed genes, we found that the expression of PTX3 was significantly up-regulated following Nogo-B over-expression as observed in lung tissues and RAW264.7 cells. In conclusion, Nogo-B plays a protective role against LPS-induced ALI, and this effect might be exerted through the modulation of alveolar macrophage recruitment and PTX3 production. |
format | Online Article Text |
id | pubmed-4502524 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | Nature Publishing Group |
record_format | MEDLINE/PubMed |
spelling | pubmed-45025242015-07-17 Nogo-B protects mice against lipopolysaccharide-induced acute lung injury Xu, Wujian Zhu, Ying Ning, Yunye Dong, Yuchao Huang, Haidong Zhang, Wei Sun, Qinying Li, Qiang Sci Rep Article Nogo-B, a member of the reticulon 4 protein family, plays a critical role in tissue repair and acute inflammation. Its role in acute lung injury (ALI) remains unclear. Here, we assessed the function of Nogo-B during tissue injury in a lipopolysaccharide (LPS)-induced ALI mouse model. We found that pulmonary Nogo-B was significantly repressed after LPS instillation in C57BL/6 mice. Over-expression of pulmonary Nogo-B using an adenovirus vector carrying the Nogo-B-RFP-3flag gene (Ad-Nogo-B) significantly prolonged the survival of mice challenged with a lethal dose of LPS. The Ad-Nogo-B-treated mice also had less severe lung injury, less alveolar protein exudation, and a higher number of macrophages but less neutrophil infiltration compared with Ad-RFP-treated mice. Interestingly, microarray analysis showed that the Ad-Nogo-B-treated mice had different gene expression profiles compared with the controls and the prominent expression of genes related to wound healing and the humoral immune response after LPS induction. Of the 49 differently expressed genes, we found that the expression of PTX3 was significantly up-regulated following Nogo-B over-expression as observed in lung tissues and RAW264.7 cells. In conclusion, Nogo-B plays a protective role against LPS-induced ALI, and this effect might be exerted through the modulation of alveolar macrophage recruitment and PTX3 production. Nature Publishing Group 2015-07-15 /pmc/articles/PMC4502524/ /pubmed/26174362 http://dx.doi.org/10.1038/srep12061 Text en Copyright © 2015, Macmillan Publishers Limited http://creativecommons.org/licenses/by/4.0/ This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ |
spellingShingle | Article Xu, Wujian Zhu, Ying Ning, Yunye Dong, Yuchao Huang, Haidong Zhang, Wei Sun, Qinying Li, Qiang Nogo-B protects mice against lipopolysaccharide-induced acute lung injury |
title | Nogo-B protects mice against lipopolysaccharide-induced acute lung injury |
title_full | Nogo-B protects mice against lipopolysaccharide-induced acute lung injury |
title_fullStr | Nogo-B protects mice against lipopolysaccharide-induced acute lung injury |
title_full_unstemmed | Nogo-B protects mice against lipopolysaccharide-induced acute lung injury |
title_short | Nogo-B protects mice against lipopolysaccharide-induced acute lung injury |
title_sort | nogo-b protects mice against lipopolysaccharide-induced acute lung injury |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4502524/ https://www.ncbi.nlm.nih.gov/pubmed/26174362 http://dx.doi.org/10.1038/srep12061 |
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