ArticleAmerican journal of respiratory cell and molecular biology2016
c-Jun Is Required for Nuclear Factor-κB-Dependent, LPS-Stimulated Fos-Related Antigen-1 Transcription in Alveolar Macrophages.
Article in American journal of respiratory cell and molecular biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 30 citations in OpenAlex.
- Non-Targeted Metabolomics Profiling and Anti-Inflammatory Potential of Star Anise Extract in Rats with Cold Stress-Aggravated Acute Lung Injury.Metabolites · 2026Article
- cJun-assisted loading of RelA DNA-binding promotes synergistic lung epithelial antimicrobial responses.iScience · 2026Article
- Integrative bioinformatics and experimental analysis reveals FRA1 as a key mediator of tubulointerstitial inflammation in lupus nephritis.Molecular medicine reports · 2026Article
- Microbiota-induced EI24 improves homeostasis but impedes function of alveolar macrophages via metabolic regulation.Nature communications · 2026Article
- Glabrol-an impurity in licorice extract-causes toxicity in muscle, bone, and immune tissues through activation of the AP-1 signaling pathway.Frontiers in pharmacology · 2026Article
- Absence of c-Maf and IL-10 enables type I IFN enhancement of innate responses to LPS in alveolar macrophages.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- Knockdown of LncRNA CCAT1 Attenuates ox-LDL-Induced Inflammation in THP1-Derived Macrophages via the miR-296-3p/FOSL1 Axis.Cardiovascular therapeutics · 2025Article
- Transcriptomic analysis reveals the key role of inflammatory and immune signaling in the anti-perimenopausal depression effects of Bushen Shugan Huayu decoction.Frontiers in psychiatry · 2025Article
- Absence of c-Maf and IL-10 enables Type I IFN enhancement of innate responses to low-dose LPS in alveolar macrophages.bioRxiv : the preprint server for biology · 2024Article
- Identification of potential miR‑155 target genes in epidermal immune microenvironment of atopic dermatitis patients and their inflammatory effects on HaCaT cells.Experimental and therapeutic medicine · 2024Article
- Article
- Fra-1 induces apoptosis and neuroinflammation by targeting S100A8 to modulate TLR4 pathways in spinal cord ischemia/reperfusion injury.Brain pathology (Zurich, Switzerland) · 2023Article
- The Fra-1: Novel role in regulating extensive immune cell states and affecting inflammatory diseases.Frontiers in immunology · 2022Review
- lncRNAMolecular therapy oncolytics · 2021Article
- Andrographolide Attenuates Established Pulmonary Hypertension via Rescue of Vascular Remodeling.Biomolecules · 2021Article
- Nrf2 Regulates Anti-InflammatoryAntioxidants (Basel, Switzerland) · 2021Article
- Lipopolysaccharide Affects the Proliferation and Glucose Metabolism of Cervical Cancer Cells Through the FRA1/MDM2/p53 Pathway.International journal of medical sciences · 2021Article
- The Transcription Factor FRA-1/AP-1 Controls Lipocalin-2 Expression and Inflammation in Sepsis Model.Frontiers in immunology · 2021Article
- Network Pharmacological Study ofBioMed research international · 2021Article
- The pathophysiology of SARS-CoV-2: A suggested model and therapeutic approach.Life sciences · 2020Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Previously, we have reported that Fos-related antigen-1 (Fra-1) transcription factor promotes LPS-induced acute lung injury and mortality, and that LPS-induced Fra-1 expression in the lung occurs predominantly in alveolar macrophages. Nuclear factor-κB (NF-κB) and c-Jun transcription factors play key roles in modulating inflammatory and immune responses induced by infectious and non-infectious insults. Here, we report that NF-κB and c-Jun coregulate Fra-1 induction by LPS in alveolar macrophages and that this regulation occurs through both the NF-κB and the extracellular signal-regulated protein kinase (ERK) signaling pathways. Transient transfections with Fra-1 promoter-reporter constructs and inhibitor studies revealed that the transcriptional activation of Fra-1 by LPS in alveolar macrophages is mediated by NF-κB and ERK1/2 signaling. Importantly, chromatin immunoprecipitation assays revealed the recruitment of c-Jun and NF-κB to the endogenous Fra-1 promoter after LPS stimulation. We found that inhibition of ERK1/2 signaling reduced LPS-stimulated c-Jun and NF-κB recruitment to the promoter. Likewise, NF-κB inhibitor blocked LPS-induced NF-κB and c-Jun binding to the promoter. ERK1/2 inhibition had no effect on c-Jun activation but suppressed LPS-stimulated NF-κB phosphorylation. Finally, functional assays showed reduced levels of LPS-stimulated NF-κB regulated proinflammatory IL-1β and macrophage inflammatory protein-1α expression and increased antiinflammatory IL-10 expression in lung alveolar macrophages of Fra-1-null mice in vivo. Thus, our studies indicate that NF-κB and c-Jun coregulate LPS-induced Fra-1 transcription and that Fra-1 selectively modulates LPS-stimulated inflammatory cytokine expression in lung alveolar macrophages during inflammatory lung injury.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.