ArticleAmerican journal of respiratory cell and molecular biology2009
Surfactant-associated protein B is critical to survival in nickel-induced injury in mice.
Article in American journal of respiratory cell and molecular biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 19 citations in OpenAlex.
- Identification of differentially expressed proteins in the injured lung from zinc chloride smoke inhalation based on proteomics analysis.Respiratory research · 2019Article
- Human pluripotent stem cell-derived alveolar epithelial cells are alternatives for in vitro pulmotoxicity assessment.Scientific reports · 2019Article
- Functional genomic assessment of phosgene-induced acute lung injury in mice.American journal of respiratory cell and molecular biology · 2013Article
- Integrative assessment of chlorine-induced acute lung injury in mice.American journal of respiratory cell and molecular biology · 2012Article
- JUN-CCAAT/enhancer-binding protein complexes inhibit surfactant-associated protein B promoter activity.American journal of respiratory cell and molecular biology · 2011Article
- Haplotype association mapping of acute lung injury in mice implicates activin a receptor, type 1.American journal of respiratory and critical care medicine · 2011Article
- Genome-wide analysis of the mouse lung transcriptome reveals novel molecular gene interaction networks and cell-specific expression signatures.Respiratory research · 2011Article
- Endothelial dysfunction and claudin 5 regulation during acrolein-induced lung injury.American journal of respiratory cell and molecular biology · 2011Article
- Mesenchymal cell survival in airway and interstitial pulmonary fibrosis.Fibrogenesis & tissue repair · 2010Article
- Gene expression profiles characterize inflammation stages in the acute lung injury in mice.PloS one · 2010Article
- Functional genomics of chlorine-induced acute lung injury in mice.Proceedings of the American Thoracic Society · 2010Article
- Genetic polymorphisms associated with acute lung injury.Pharmacogenomics · 2009Review
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Authors and funding
19 authors at 5 institutions in 1 country.
Funding
Abstract
The etiology of acute lung injury is complex and associated with numerous, chemically diverse precipitating factors. During acute lung injury in mice, one key event is epithelial cell injury that leads to reduced surfactant biosynthesis. We have previously reported that transgenic mice that express transforming growth factor alpha (TGFA) in the lung were protected during nickel-induced lung injury. Here, we find that the mechanism by which TGFA imparts protection includes maintenance of surfactant-associated protein B (SFTPB) transcript levels and epidermal growth factor receptor-dependent signaling in distal pulmonary epithelial cells. This protection is complex and not accompanied by a diminution in inflammatory mediator transcripts or additional stimulation of antioxidant transcripts. In mouse lung epithelial (MLE-15) cells, microarray analysis demonstrated that nickel increased transcripts of genes enriched in MTF1, E2F-1, and AP-2 transcription factor-binding sites and decreased transcripts of genes enriched in AP-1-binding sites. Nickel also increased Jun transcript and DNA-binding activity, but decreased SFTPB transcript. Expression of SFTPB under the control of a doxycycline-sensitive promoter increased survival during nickel-induced injury as compared with control mice. Together, these findings support the idea that maintenance of SFTPB expression is critical to survival during acute lung injury.
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