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Nogo-B protects mice against lipopolysaccharide-induced acute lung injury.

Xu W, Zhu Y, Ning Y, Dong Y, Huang H, Zhang W, Sun Q, Li Q - Sci Rep (2015)

Bottom Line: Nogo-B, a member of the reticulon 4 protein family, plays a critical role in tissue repair and acute inflammation.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.

View Article: PubMed Central - PubMed

Affiliation: 1] Department of Respiratory Disease, Changhai Hospital, Second Military Medical University, China [2] Department of Respiratory Medicine, Jinling Hospital, Nanjing, China.

ABSTRACT
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.

No MeSH data available.


Related in: MedlinePlus

Effects of Nogo-B over-expression on gene expression profiles after LPS instillation in C57BL/6 mice.(A) Principal component analysis showed that the gene expression profiles were separated based on Ad-Nogo-B transfection after LPS induction. (B) Hierarchical clustering analysis demonstrated that the gene expression patterns were highly dependent on LPS induction and were affected by Nogo-B over-expression.
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f5: Effects of Nogo-B over-expression on gene expression profiles after LPS instillation in C57BL/6 mice.(A) Principal component analysis showed that the gene expression profiles were separated based on Ad-Nogo-B transfection after LPS induction. (B) Hierarchical clustering analysis demonstrated that the gene expression patterns were highly dependent on LPS induction and were affected by Nogo-B over-expression.

Mentions: To further determine the mechanisms by which Nogo-B is modulated in LPS-induced lung injury, microarray was performed to detect differentially expressed genes between the mice transfected with either Ad-Nogo-B or Ad-RFP and subsequently treated with or without LPS (15 mg/kg). PCA and clustering analysis showed that the overall gene profiles were separated based on Ad-Nogo-B transfection after LPS induction but not before LPS induction (Fig. 5A-B). After LPS induction, the Ad-RFP-treated mice showed a total of 1,988 differentially expressed genes. Of these genes, gene ontology analysis revealed those assigned to the biological process subontology were mainly involved in locomotory behavior and the inflammatory response (Table 2).The Ad-Nogo-B-treated mice showed 1,645 differentially expressed genes after LPS instillation. Gene ontology analysis revealed that these genes were involved in locomotory behavior and the inflammatory response, in addition to the response to wounding, response to external stimulus and humoral immune response (Table 2), suggesting that Nogo-B over-expression exerts a broader effect on the pathophysiology of LPS-induced ALI.


Nogo-B protects mice against lipopolysaccharide-induced acute lung injury.

Xu W, Zhu Y, Ning Y, Dong Y, Huang H, Zhang W, Sun Q, Li Q - Sci Rep (2015)

Effects of Nogo-B over-expression on gene expression profiles after LPS instillation in C57BL/6 mice.(A) Principal component analysis showed that the gene expression profiles were separated based on Ad-Nogo-B transfection after LPS induction. (B) Hierarchical clustering analysis demonstrated that the gene expression patterns were highly dependent on LPS induction and were affected by Nogo-B over-expression.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4502524&req=5

f5: Effects of Nogo-B over-expression on gene expression profiles after LPS instillation in C57BL/6 mice.(A) Principal component analysis showed that the gene expression profiles were separated based on Ad-Nogo-B transfection after LPS induction. (B) Hierarchical clustering analysis demonstrated that the gene expression patterns were highly dependent on LPS induction and were affected by Nogo-B over-expression.
Mentions: To further determine the mechanisms by which Nogo-B is modulated in LPS-induced lung injury, microarray was performed to detect differentially expressed genes between the mice transfected with either Ad-Nogo-B or Ad-RFP and subsequently treated with or without LPS (15 mg/kg). PCA and clustering analysis showed that the overall gene profiles were separated based on Ad-Nogo-B transfection after LPS induction but not before LPS induction (Fig. 5A-B). After LPS induction, the Ad-RFP-treated mice showed a total of 1,988 differentially expressed genes. Of these genes, gene ontology analysis revealed those assigned to the biological process subontology were mainly involved in locomotory behavior and the inflammatory response (Table 2).The Ad-Nogo-B-treated mice showed 1,645 differentially expressed genes after LPS instillation. Gene ontology analysis revealed that these genes were involved in locomotory behavior and the inflammatory response, in addition to the response to wounding, response to external stimulus and humoral immune response (Table 2), suggesting that Nogo-B over-expression exerts a broader effect on the pathophysiology of LPS-induced ALI.

Bottom Line: Nogo-B, a member of the reticulon 4 protein family, plays a critical role in tissue repair and acute inflammation.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.

View Article: PubMed Central - PubMed

Affiliation: 1] Department of Respiratory Disease, Changhai Hospital, Second Military Medical University, China [2] Department of Respiratory Medicine, Jinling Hospital, Nanjing, China.

ABSTRACT
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.

No MeSH data available.


Related in: MedlinePlus