ArticleAmerican journal of physiology. Lung cellular and molecular physiology2015
CXCL8 histone H3 acetylation is dysfunctional in airway smooth muscle in asthma: regulation by BET.
Article in American journal of physiology. Lung cellular and molecular physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
38 citing papers in PubMed, 1 synthesis or guideline pooled it, 66 citations in OpenAlex.
- Meta-analysis of microarray data to identify potential signature genes and MiRNAs associated with the pathogenesis of asthma.Journal of translational medicine · 2025Pooled it
- Glycolytic reprogramming and cell-specific lactylation in asthma: an evidence-graded framework for testable metabolic-epigenetic profiles.Frontiers in immunology · 2026Review
- Structural and Functional Studies on Key Epigenetic Regulators in Asthma.Biomolecules · 2025Review
- Unmasking Pediatric Asthma: Epigenetic Fingerprints and Markers of Respiratory Infections.International journal of molecular sciences · 2025Review
- Developmental air pollution exposure augments airway hyperreactivity, alters transcriptome, and DNA methylation in female adult progeny.Communications biology · 2025Article
- Identification of SIN3A as a Promising Epigenetic Target Against Allergic Rhinitis.Journal of inflammation research · 2025Article
- Exploring potential therapeutic targets for asthma: a proteome-wide Mendelian randomization analysis.Journal of translational medicine · 2024Article
- SNORA28 Promotes Proliferation and Radioresistance in Colorectal Cancer Cells through the STAT3 Pathway by Increasing H3K9 Acetylation in the LIFR Promoter.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Transcriptional co-activators: emerging roles in signaling pathways and potential therapeutic targets for diseases.Signal transduction and targeted therapy · 2023Review
- BRD4 as a Therapeutic Target in Pulmonary Diseases.International journal of molecular sciences · 2023Review
- Bioinformatic analysis and experimental validation of the potential gene in the airway inflammation of steroid-resistant asthma.Scientific reports · 2023Article
- Pathogenesis of allergic diseases and implications for therapeutic interventions.Signal transduction and targeted therapy · 2023Review
- CXCL8 and the peritoneal metastasis of ovarian and gastric cancer.Frontiers in immunology · 2023Review
- Cellular sources of airway smooth muscle cells in asthmatic airway remodeling and their clinical relevance: a narrative review.Annals of translational medicine · 2022Article
- Epigenetic Mechanisms in Allergy Development and Prevention.Handbook of experimental pharmacology · 2022Article
- Pathobiology of Airway Remodeling in Asthma: The Emerging Role of Integrins.Journal of asthma and allergy · 2022Review
- Current understanding of epigenetics in atopic dermatitis.Experimental dermatology · 2021Review
- A review of epigenetic changes in asthma: methylation and acetylation.Clinical epigenetics · 2021Review
- Insights into glucocorticoid responses derived from omics studies.Pharmacology & therapeutics · 2021Review
- The BET family in immunity and disease.Signal transduction and targeted therapy · 2021Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Asthma is characterized by airway inflammation and remodeling and CXCL8 is a CXC chemokine that drives steroid-resistant neutrophilic airway inflammation. We have shown that airway smooth muscle (ASM) cells isolated from asthmatic individuals secrete more CXCL8 than cells from nonasthmatic individuals. Here we investigated chromatin modifications at the CXCL8 promoter in ASM cells from nonasthmatic and asthmatic donors to further understand how CXCL8 is dysregulated in asthma. ASM cells from asthmatic donors had increased histone H3 acetylation, specifically histone H3K18 acetylation, and increased binding of histone acetyltransferase p300 compared with nonasthmatic donors but no differences in CXCL8 DNA methylation. The acetylation reader proteins Brd3 and Brd4 were bound to the CXCL8 promoter and Brd inhibitors inhibited CXCL8 secretion from ASM cells by disrupting Brd4 and RNA polymerase II binding to the CXCL8 promoter. Our results show a novel dysregulation of CXCL8 transcriptional regulation in asthma characterized by a promoter complex that is abnormal in ASM cells isolated from asthmatic donors and can be modulated by Brd inhibitors. Brd inhibitors may provide a new therapeutic strategy for steroid-resistant inflammation.
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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.