ArticleRespiratory research2024
Expression of glucocorticoid receptor and HDACs in airway smooth muscle cells is associated with response to steroids in COPD.
Article in Respiratory research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Research progress on lysine acetylation (Review).International journal of molecular medicine · 2026Review
- Balancing inflammation under stress: glucocorticoid regulation of innate immune pathways.Bioscience reports · 2026Review
- Ligand-driven modulation of chaperone-cochaperone networks shapes proteostasis outcomes.Protein science : a publication of the Protein Society · 2026Article
- Resveratrol restores glucocorticoid receptor and HDAC2 to overcome corticosteroid resistance in cigarette smoke-induced emphysema mice.Journal of thoracic disease · 2025Article
- Two heads are better than one: a synergistic strategy for conquering graft-Haematologica · 2025Article
- Glucocorticoid Insensitivity: Is It a Question of Time and Place?Biomedicines · 2025Review
- Integrative Roles of Pro-Inflammatory Cytokines on Airway Smooth Muscle Structure and Function in Asthma.Immunological reviews · 2025Review
- Long-Term Cigarette Smoke Exposure Promotes Neutrophil Ferroptosis Resistance, Inducing Neutrophil Extracellular Trap Formation and Driving Glucocorticoid Resistance in Chronic Obstructive Pulmonary Disease.Research (Washington, D.C.) · 2025Article
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5 authors.
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Abstract
backgroundSteroid insensitivity in Chronic Obstructive Pulmonary Disease (COPD) presents a problem for controlling the chronic inflammation of the airways. The glucocorticoid receptor (GR) mediates the intracellular signaling of inhaled corticosteroids (ICS) by interacting with transcription factors and histone deacetylases (HDACs). The aim of this study was to assess if COPD patients' response to ICS in vivo, may be associated with the expression of GR, the complex of GR with transcription factors, and the expression of various HDACs in vitro.
methodsPrimary airway smooth muscle cells (ASMC) were established from endobronchial biopsies obtained from patients with asthma (n = 10), patients with COPD (n = 10) and subjects that underwent diagnostic bronchoscopy without pathological findings and served as controls (n = 6). ASMC were also established from 18 COPD patients, 10 responders and 8 non-responders to ICS, who participated in the HISTORIC study, an investigator-initiated and driven clinical trial that proved the hypothesis that COPD patients with high ASMC in their endobronchial biopsies respond better to ICS than patients with low ASMC. Expression of GR and its isoforms GRα and GRβ and HDACs was investigated in primary ASMC in the absence or in the presence of dexamethasone (10
resultsExpression of GR and its isoform GRα but not GRβ was significantly reduced in ASMC from COPD patients as compared to controls. There were no significant differences in the expression of GR, GRα and GRβ between responders and non-responders to ICS. However, treatment with dexamethasone upregulated the expression of total GR (p = 0.004) and GRα (p = 0.005) after 30 min in responders but not in non-responders. Τhe formation of the complex GR-c-Jun was increased 60 min after treatment with dexamethasone only in responders who exhibited significantly lower expression of HDAC3 (p = 0.005) and HDAC5 (p < 0.0001) as compared to non-responders.
conclusionsThese data suggest that ASMC from COPD patients who do not respond to treatment with ICS, are characterized by reduced GR-c-Jun complex formation and increased expression of HDAC3 and HDAC5.
trial registrationISRCTN11017699 (Registration date: 15/11/2016).
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