ArticleBritish journal of pharmacology2005
Stimulus-dependent glucocorticoid-resistance of GM-CSF production in human cultured airway smooth muscle.
Article in British journal of pharmacology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
15 citing papers in PubMed, 33 citations in OpenAlex.
- Analysis of alpha-1-antitrypsin (AAT)-regulated, glucocorticoid receptor-dependent genes in macrophages reveals a novel host defense function of AAT.Physiological reports · 2024Article
- Pathogenesis of allergic diseases and implications for therapeutic interventions.Signal transduction and targeted therapy · 2023Review
- Integrated multi-omics analyses reveal the altered transcriptomic characteristics of pulmonary macrophages in immunocompromised hosts withFrontiers in immunology · 2023Article
- Glucocorticoid Insensitivity in Asthma: The Unique Role for Airway Smooth Muscle Cells.International journal of molecular sciences · 2022Review
- Important lessons learned from studies on the pharmacology of glucocorticoids in human airway smooth muscle cells: Too much of a good thing may be a problem.Pharmacology & therapeutics · 2020Review
- Understanding how long-acting βBritish journal of pharmacology · 2016Review
- NF-kappaB Signaling in Chronic Inflammatory Airway Disease.Biomolecules · 2015Review
- The inflammatory actions of coagulant and fibrinolytic proteases in disease.Mediators of inflammation · 2015Review
- Mechanisms of suppression of alveolar epithelial cell GM-CSF expression in the setting of hyperoxic stress.American journal of physiology. Lung cellular and molecular physiology · 2010Article
- Airway smooth muscle as an immunomodulatory cell.Pulmonary pharmacology & therapeutics · 2009Review
- Regulation of inflammation by airway smooth muscle.Current allergy and asthma reports · 2008Review
- Airway smooth muscle cell as an inflammatory cell: lessons learned from interferon signaling pathways.Proceedings of the American Thoracic Society · 2008Review
- Airway smooth muscle dynamics: a common pathway of airway obstruction in asthma.The European respiratory journal · 2007Review
- Collagen impairs glucocorticoid actions in airway smooth muscle through integrin signalling.British journal of pharmacology · 2006Article
- Endogenous laminin is required for human airway smooth muscle cell maturation.Respiratory research · 2006Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
For a subpopulation of asthmatics, symptoms persist even with high doses of glucocorticoids. Glucocorticoids reduce the levels of the proinflammatory and fibrogenic cytokine, granulocyte-macrophage colony-stimulating factor (GM-CSF) produced by human cultured airway smooth muscle (ASM). We have contrasted the effects of a synthetic glucocorticoid, dexamethasone, on thrombin- and IL-1alpha-stimulated GM-CSF production in human ASM cells. Although IL-1alpha stimulated three-fold higher levels of GM-CSF mRNA and protein compared to thrombin, dexamethasone concentration-dependently reduced IL-1alpha-stimulated GM-CSF more potently and to a greater extent than the response to thrombin. This pattern of glucocorticoid regulation was also observed at the GM-CSF mRNA level and was reproduced with other glucocorticoids such as fluticasone propionate. IL-1alpha and thrombin stimulated NF-kappa B-dependent luciferase expression equally. Dexamethasone treatment reduced luciferase expression stimulated by both IL-1alpha and thrombin. The GM-CSF mRNA half life was markedly prolonged by IL-1alpha compared to thrombin. This IL-1alpha-induced GM-CSF mRNA stability was prevented by either dexamethasone or the p38(MAPK) inhibitor, SB203580, neither of which influenced GM-CSF mRNA stability in thrombin-treated cells. Dexamethasone inhibited p38(MAPK) phosphorylation in IL-1alpha-stimulated ASM, whereas thrombin does not stimulate p38(MAPK) phosphorylation. These data suggest that the mechanism underlying the greater potency and efficacy of glucocorticoids in reducing GM-CSF synthesis stimulated by IL-1alpha depends on inhibition of the involvement of p38(MAPK)-induced increases in GM-CSF message stability.
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Registered trials
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