ArticleThe Journal of biological chemistry2015
BET bromodomains regulate transforming growth factor-β-induced proliferation and cytokine release in asthmatic airway smooth muscle.
Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 55 citations in OpenAlex.
- From allergens to epigenetics: how histone acetylation shapes immune gene expression in allergic diseases.Epigenomics · 2025Review
- BRD4 as a Therapeutic Target in Pulmonary Diseases.International journal of molecular sciences · 2023Review
- Cellular sources of airway smooth muscle cells in asthmatic airway remodeling and their clinical relevance: a narrative review.Annals of translational medicine · 2022Article
- Curcumin modulates airway remodelling-contributing genes-the significance of transcription factors.Journal of cellular and molecular medicine · 2022Article
- Epigenetic Mechanisms in Allergy Development and Prevention.Handbook of experimental pharmacology · 2022Article
- The BET family in immunity and disease.Signal transduction and targeted therapy · 2021Review
- BRD4 inhibition alleviates mechanical stress-induced TMJ OA-like pathological changes and attenuates TREM1-mediated inflammatory response.Clinical epigenetics · 2021Article
- Airway Epithelial Cells Drive Airway Smooth Muscle Cell Phenotype Switching to the Proliferative and Pro-inflammatory Phenotype.Frontiers in physiology · 2021Article
- BETs that cover the spread from acquired to heritable heart failure.The Journal of clinical investigation · 2020Article
- BET bromodomain proteins regulate transcriptional reprogramming in genetic dilated cardiomyopathy.JCI insight · 2020Article
- BET Epigenetic Reader Proteins in Cardiovascular Transcriptional Programs.Circulation research · 2020Review
- Let-7a inhibits proliferation and promotes apoptosis of human asthmatic airway smooth muscle cells.Experimental and therapeutic medicine · 2019Article
- Epigenetic impacts of maternal tobacco and e-vapour exposure on the offspring lung.Clinical epigenetics · 2019Review
- Function of BRD4 in the pathogenesis of high glucose‑induced cardiac hypertrophy.Molecular medicine reports · 2019Article
- BETting on Novel Treatments for Asthma: Bromodomain 4 Inhibitors.American journal of respiratory cell and molecular biology · 2019Article
- The anti-proliferative and anti-inflammatory response of COPD airway smooth muscle cells to hydrogen sulfide.Respiratory research · 2018Article
- Histone modifications and their role in epigenetics of atopy and allergic diseases.Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · 2018Review
- Aberrant control of NF-κB in cancer permits transcriptional and phenotypic plasticity, to curtail dependence on host tissue: molecular mode.Cancer biology & medicine · 2017Article
- Transcriptional profiling identifies the long noncoding RNA plasmacytoma variant translocation (PVT1) as a novel regulator of the asthmatic phenotype in human airway smooth muscle.The Journal of allergy and clinical immunology · 2017Article
- Bromodomain and Extra-Terminal Protein Inhibition Attenuates Neutrophil-dominant Allergic Airway Disease.Scientific reports · 2017Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Airway smooth muscle (ASM) mass is increased in asthma, and ASM cells from patients with asthma are hyperproliferative and release more IL-6 and CXCL8. The BET (bromo- and extra-terminal) family of proteins (Brd2, Brd3, and Brd4) govern the assembly of histone acetylation-dependent chromatin complexes. We have examined whether they modulate proliferation and cytokine expression in asthmatic ASM cells by studying the effect of BET bromodomain mimics JQ1/SGCBD01 and I-BET762. ASM cells from healthy individuals and nonsevere and severe asthmatics were pretreated with JQ1/SGCBD01 and I-BET762 prior to stimulation with FCS and TGF-β. Proliferation was measured by BrdU incorporation. IL-6 and CXCL8 release was measured by ELISA, and mRNA expression was measured by quantitative RT-PCR. ChIP using a specific anti-Brd4 antibody and PCR primers directed against the transcriptional start site of IL-6 and CXCL8 gene promoters was performed. Neither JQ1/SGCBD01 nor I-BET762 had any effect on ASM cell viability. JQ1/SGCBD01 and I-BET762 inhibited FCS+TGF-β-induced ASM cell proliferation and IL-6 and CXCL8 release in healthy individuals (≥ 30 nM) and in nonsevere and severe asthma patients (≥100 nM), with the latter requiring higher concentrations of these mimics. JQ1/SGCBD01 reduced Brd4 binding to IL8 and IL6 promoters induced by FCS+TGF-β. Mimics of BET bromodomains inhibit aberrant ASM cell proliferation and inflammation with lesser efficiency in those from asthmatic patients. They may be effective in reducing airway remodeling in asthma.
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