ArticleOncogene2011
Interstitial lung disease induced by gefitinib and toll-like receptor ligands is mediated by Fra-1.
Article in Oncogene, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 26 citations in OpenAlex.
- Overexpression of FRA1 (Cells · 2023Article
- Bioinformatic and systems biology approach revealing the shared genes and molecular mechanisms between COVID-19 and non-alcoholic hepatitis.Frontiers in molecular biosciences · 2023Article
- Role of the Transcription Factor FOSL1 in Organ Development and Tumorigenesis.International journal of molecular sciences · 2022Review
- The Fra-1: Novel role in regulating extensive immune cell states and affecting inflammatory diseases.Frontiers in immunology · 2022Review
- FOSL1 is a novel mediator of endotoxin/lipopolysaccharide-induced pulmonary angiogenic signaling.Scientific reports · 2020Article
- Fos-related antigen-1 transgenic mouse as a model for systemic sclerosis: A potential role of M2 polarization.Journal of scleroderma and related disorders · 2019Article
- Transcription factor Fra-1 targets arginase-1 to enhance macrophage-mediated inflammation in arthritis.The Journal of clinical investigation · 2019Article
- c-Jun Is Required for Nuclear Factor-κB-Dependent, LPS-Stimulated Fos-Related Antigen-1 Transcription in Alveolar Macrophages.American journal of respiratory cell and molecular biology · 2016Article
- Visualization of Fra-1/AP-1 activation during LPS-induced inflammatory lung injury using fluorescence optical imaging.American journal of physiology. Lung cellular and molecular physiology · 2015Article
- Expression profiling of genes regulated by Fra-1/AP-1 transcription factor during bleomycin-induced pulmonary fibrosis.BMC genomics · 2013Article
- Article
- Oxidant-induced cell death and Nrf2-dependent antioxidative response are controlled by Fra-1/AP-1.Molecular and cellular biology · 2012Article
- Genetic disruption of Fra-1 decreases susceptibility to endotoxin-induced acute lung injury and mortality in mice.American journal of respiratory cell and molecular biology · 2012Article
- Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The role of the AP-1 transcription factor Fra-1 (encoded by Fosl1) in inflammatory responses associated with lung disease is largely unknown. Here, we show that Fra-1 overexpression in mice reduced proinflammatory cytokine production in response to injection of lipopolysaccharide (LPS), a Toll-like receptor (TLR)-ligand. Unexpectedly, Fra-1 transgenic mice died rapidly following LPS treatment, showing severe interstitial lung disease and displaying massive accumulation of macrophages and overproduction of several chemokines, including macrophage chemoattractant protein-1 (MCP-1, encoded by Ccl2). To assess the clinical relevance of Fra-1 in lung pathology, mice were treated with the anticancer drug gefitinib (Iressa), which can lead to interstitial lung disease in patients. Gefitinib-treated mice showed increased Fosl1 and Ccl2 expression and developed interstitial lung disease in response to LPS, endogenous TLR ligands and chemotherapy. Moreover, deletion of Fra-1 or blocking MCP-1 receptor signaling in mice attenuated gefitinib-enhanced lethality in response to LPS. Importantly, human alveolar macrophages showed enhanced LPS-induced FOSL1 and CCL2 expression after gefitinib treatment. These results indicate that Fra-1 is an important mediator of interstitial lung disease following gefitinib treatment.
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Registered trials
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