ArticleAmerican journal of respiratory cell and molecular biology2012
Genetic disruption of Fra-1 decreases susceptibility to endotoxin-induced acute lung injury and mortality in mice.
Article in American journal of respiratory cell and molecular biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 26 citations in OpenAlex.
- Mesenchymal stem cells-derived TGF-β1 promotes polarization of M2 macrophages in mice with acute-on-chronic liver failure via FOSL1/MERTK axis.Stem cell research & therapy · 2026Article
- FRA1 (Frontiers in cell and developmental biology · 2025Article
- FOSL1's Oncogene Roles in Glioma/Glioma Stem Cells and Tumorigenesis: A Comprehensive Review.International journal of molecular sciences · 2024Review
- Bioinformatic and systems biology approach revealing the shared genes and molecular mechanisms between COVID-19 and non-alcoholic hepatitis.Frontiers in molecular biosciences · 2023Article
- Functional reprogramming of monocytes in patients with acute and convalescent severe COVID-19.JCI insight · 2022Article
- 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
- Silencing lncRNA AGAP2-AS1 Upregulates miR-195-5p to Repress Migration and Invasion of EC Cells via the Decrease of FOSL1 Expression.Molecular therapy. Nucleic acids · 2020Article
- Transcription factor-mediated signaling pathways' contribution to the pathology of acute lung injury and acute respiratory distress syndrome.American journal of translational research · 2020Article
- 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
- Myeloid-specific Fos-related antigen-1 regulates cigarette smoke-induced lung inflammation, not emphysema, in mice.American journal of respiratory cell and molecular biology · 2015Article
- Oxidant-induced cell death and Nrf2-dependent antioxidative response are controlled by Fra-1/AP-1.Molecular and cellular biology · 2012Article
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4 authors at 1 institution in 1 country.
Funding
Abstract
The activator protein-1 (AP-1) transcription factor, comprising Jun and Fos family proteins, distinctly regulates various cellular processes, including those involved in inflammation. FOS like antigen 1 (Fra-1), a member of the Fos family, dimerizes with members of the Jun family and regulates gene expression in a context-dependent manner. Although respiratory toxicants are known to stimulate the expression of Fra-1 in the lung, whether Fra-1 promotes or decreases susceptibility to the development and progression of toxicant-induced lung disease in vivo is not well established. To determine the role of Fra-1 in LPS-induced acute lung injury and mortality, we administered LPS either intraperitoneally or intratracheally to Fra-1-sufficient (Fra-11(+/+)) and Fra-1-deficient (Fra-1(Δ/Δ)) mice. LPS-induced mortality, lung injury, inflammation, cytokine measurements, and AP-1 and NF-κB activities were then assessed in these mice. Fra-1(Δ/Δ) mice showed a greater resistance to LPS-induced mortality than did their Fra-1(+/+) counterparts. Consistent with this result, LPS-induced lung injury and inflammatory responses were markedly lower in Fra-1(Δ/Δ) mice than in Fra-1(+/+) mice. Compared with Fra-1(+/+) mice, Fra-1(Δ/Δ) mice showed a reduced influx of neutrophils into the lungs, accompanied by a decreased expression of proinflammatory cytokines in response to treatment with LPS. The decreased inflammatory responses in Fra-1(Δ/Δ) mice coincided with diminished and increased levels of NF-κB and c-Jun/AP-1 binding, respectively. These results demonstrate that Fra-1/AP-1 plays a key role in promoting LPS-induced injury and mortality in mice, and they suggest that targeting (i.e., inhibiting) this transcription factor may be a useful approach to dampening the adverse effects of exposure to endotoxins.
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