ArticleMucosal immunology2012
c-Ets1 inhibits the interaction of NF-κB and CREB, and downregulates IL-1β-induced MUC5AC overproduction during airway inflammation.
Article in Mucosal immunology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 18 citations in OpenAlex.
- ETS Transcription Factors in Immune Cells and Immune-Related Diseases.International journal of molecular sciences · 2024Review
- Brief research report: ETS-1 blockade increases ICAM-1 expression in activated human retinal endothelial cells.Frontiers in ophthalmology · 2024Article
- IL-1β Promotes Expansion of IL-33American journal of respiratory cell and molecular biology · 2022Article
- Endoplasmic reticulum stress/XBP1 promotes airway mucin secretion under the influence of neutrophil elastase.International journal of molecular medicine · 2021Article
- Andrographolide sulfate inhibited NF-κB activation and alleviated pneumonia induced by poly I:C in mice.Journal of pharmacological sciences · 2020Article
- MiR-532-5p suppresses renal cancer cell proliferation by disrupting the ETS1-mediated positive feedback loop with the KRAS-NAP1L1/P-ERK axis.British journal of cancer · 2018Article
- Article
- Regulation of Airway Inflammation by G-protein Regulatory Motif Peptides of AGS3 protein.Scientific reports · 2016Article
- Association of E26 Transformation Specific Sequence 1 Variants with Rheumatoid Arthritis in Chinese Han Population.PloS one · 2015Article
- Role of p38 MAPK and STAT3 in lipopolysaccharide-stimulated mouse alveolar macrophages.Experimental and therapeutic medicine · 2014Article
- IL-1β induction of MUC5AC gene expression is mediated by CREB and NF-κB and repressed by dexamethasone.American journal of physiology. Lung cellular and molecular physiology · 2014Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mucin hypersecretion is frequently observed in many inflammatory diseases of the human respiratory tract. As mucin hypersecretion refers to uncontrolled mucin expression and secretion during inflammation, studies examining the negative control mechanisms of mucin hypersecretion are vital in developing novel therapeutic medications. We hypothesized that the c-Ets1 induced by interleukin (IL)-1β would decrease MUC5AC overproduction by inhibiting the interaction of NF-κB with cAMP response element-binding protein (CREB) in vivo. Stimulation with IL-1β caused the direct binding of NF-κB and CREB to the MUC5AC promoter, thus increasing MUC5AC gene expression. However, IL-1β-induced MUC5AC messenger RNA levels were surprizingly downregulated by c-Ets1 (located -938 to -930). Interestingly, c-Ets1 also suppressed IL-1β-induced MUC5AC gene expression in vitro and in vivo by disrupting the interaction of NF-κB with CREB on the MUC5AC promoter. In addition, c-Ets1 also inhibited significant morphologic changes and inflammatory cell infiltration after IL-1β exposure in mouse lungs infected with either wild-type or shRNA-c-Ets1. Moreover, reactive oxygen species produced by NOX4 increased c-Ets1 gene expression and MUC5AC gene expression in alveolar macrophages from bronchoalveolar lavage fluid. These results suggest a molecular paradigm for the establishment of a novel mechanism underlying the negative regulation of mucin overproduction, thus enhancing our understanding of airway inflammation.
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