ArticleAmerican journal of respiratory cell and molecular biology2009
Glucocorticoid- and protein kinase A-dependent transcriptome regulation in airway smooth muscle.
Article in American journal of respiratory cell and molecular biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
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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
28 citing papers in PubMed, 43 citations in OpenAlex.
- Computational Investigation of Smooth Muscle Cell Plasticity in Atherosclerosis and Vascular Calcification: Insights from Differential Gene Expression Analysis of Microarray Data.Bioengineering (Basel, Switzerland) · 2025Article
- Integrative Roles of Pro-Inflammatory Cytokines on Airway Smooth Muscle Structure and Function in Asthma.Immunological reviews · 2025Review
- Regulation of Airway Smooth Muscle Cell Proliferation by Diacylglycerol Kinase: Relevance to Airway Remodeling in Asthma.International journal of molecular sciences · 2022Article
- CEBPD modulates the airway smooth muscle transcriptomic response to glucocorticoids.Respiratory research · 2022Article
- 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
- The proton-sensing receptor ovarian cancer G-protein coupled receptor 1 (OGR1) in airway physiology and disease.Current opinion in pharmacology · 2020Review
- Whole Genome Sequencing Identifies CRISPLD2 as a Lung Function Gene in Children With Asthma.Chest · 2019Article
- Specificity of NHERF1 regulation of GPCR signaling and function in human airway smooth muscle.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- Airway Smooth Muscle-Specific Transcriptomic Signatures of Glucocorticoid Exposure.American journal of respiratory cell and molecular biology · 2019Article
- Using omics approaches to understand pulmonary diseases.Respiratory research · 2017Review
- Gene expression effects of glucocorticoid and mineralocorticoid receptor agonists and antagonists on normal human skeletal muscle.Physiological genomics · 2017Article
- Understanding how long-acting βBritish journal of pharmacology · 2016Review
- Glucocorticoid and TNF signaling converge at A20 (TNFAIP3) to repress airway smooth muscle cytokine expression.American journal of physiology. Lung cellular and molecular physiology · 2016Article
- Antimitogenic effect of bitter taste receptor agonists on airway smooth muscle cells.American journal of physiology. Lung cellular and molecular physiology · 2016Article
- IL-6 trans-signaling increases expression of airways disease genes in airway smooth muscle.American journal of physiology. Lung cellular and molecular physiology · 2015Article
- A-kinase-anchoring proteins coordinate inflammatory responses to cigarette smoke in airway smooth muscle.American journal of physiology. Lung cellular and molecular physiology · 2015Article
- Article
- A-kinase anchoring proteins regulate compartmentalized cAMP signaling in airway smooth muscle.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2012Article
- Genome-wide association analysis in asthma subjects identifies SPATS2L as a novel bronchodilator response gene.PLoS genetics · 2012Article
- How can microarrays unlock asthma?Journal of allergy · 2012Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Glucocorticoids (GCs) and protein kinase A (PKA)-activating agents (beta-adrenergic receptor agonists) are mainstream asthma therapies based on their ability to prevent or reverse excessive airway smooth muscle (ASM) constriction. Their abilities to regulate another important feature of asthma--excessive ASM growth--are poorly understood. Recent studies have suggested that GCs render agents of inflammation such as IL-1 beta and TNF-alpha mitogenic to ASM, via suppression of (antimitogenic) induced cyclooxygenase-2-dependent PKA activity. To further explore the mechanistic basis of these observations, we assessed the effects of epidermal growth factor and IL-1 beta stimulation, and the modulatory effects of GC treatment and PKA inhibition, on the ASM transcriptome by microarray analysis. Results demonstrate that ASM stimulated with IL-1 beta, in a manner that is often cooperative with stimulation with epidermal growth factor, exhibit a profound capacity to function as immunomodulatory cells. Moreover, results implicate an important role for induced autocrine/paracrine factors (many whose regulation was minimally affected by GCs or PKA inhibition) as regulators of both airway inflammation and ASM growth. Induction of numerous chemokines, in conjunction with regulation of proteases and agents of extracellular matrix remodeling, is suggested as an important mechanism promoting upregulated G protein-coupled receptor signaling capable of stimulating ASM growth. Additional functional assays suggest that intracellular PKA plays a critical role in suppressing the promitogenic effects of induced autocrine factors in ASM. Finally, identification and comparison of GC- and PKA-sensitive genes in ASM provide insight into the complementary effects of beta-agonist/GC combination therapies, and suggest specific genes as important targets for guiding the development of new generations of GCs and adjunct asthma therapies.
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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.