ArticleScientific reports2015
Nogo-B protects mice against lipopolysaccharide-induced acute lung injury.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.
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Who cites it
9 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.
- Gene Expression Analysis to Assess the Relevance of Rodent Models to Human Lung Injury.American journal of respiratory cell and molecular biology · 2017Pooled it
- Reticulon 2 promotes gastric cancer metastasis via activating endoplasmic reticulum CaCell death & disease · 2022Article
- Long noncoding RNA Kcnq1ot1 prompts lipopolysaccharide-induced acute lung injury by microRNA-7a-5p/Rtn3 axis.European journal of medical research · 2022Article
- Inhibition of miR-29b-1-5p Attenuates Inflammatory Response and Pulmonary Fibrosis in LPS-Induced Acute Lung Injury by Regulating RTN4 Expression.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Nogo-B promotes epithelial-mesenchymal transition in lung fibrosis via PERK branch of the endoplasmic reticulum stress pathway.Annals of translational medicine · 2021Article
- Ameliorative Effect of Thymoquinone-Loaded PLGA Nanoparticles on Chronic Lung Injury Induced by Repetitive Intratracheal Instillation of Lipopolysaccharide in Rats.Oxidative medicine and cellular longevity · 2021Article
- Mitochondria-Modulating Porous Se@SiOInternational journal of nanomedicine · 2020Article
- Transplantation of HUVECs with genetically modified Nogo-B accelerates wound-healing in nude mice.American journal of translational research · 2019Article
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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.
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