ArticleBritish journal of pharmacology2011
Protein kinase A and the exchange protein directly activated by cAMP (Epac) modulate phenotype plasticity in human airway smooth muscle.
Article in British journal of pharmacology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 28 citations in OpenAlex.
- Comparing DNA methylation profiles across different tissues associated with the diagnosis of pediatric asthma.Scientific reports · 2020Article
- Disruption of AKAP-PKA Interaction Induces Hypercontractility With Concomitant Increase in Proliferation Markers in Human Airway Smooth Muscle.Frontiers in cell and developmental biology · 2020Article
- Exchange protein directly activated by cAMP (Epac) protects against airway inflammation and airway remodeling in asthmatic mice.Respiratory research · 2019Article
- Review
- Selective small-molecule EPAC activators.Biochemical Society transactions · 2019Review
- Genome-Wide Mapping Defines a Role for C/EBPβ and c-Jun in Non-Canonical Cyclic AMP Signalling.Cells · 2019Article
- Intracellular cAMP Sensor EPAC: Physiology, Pathophysiology, and Therapeutics Development.Physiological reviews · 2018Review
- The Potential of a Novel Class of EPAC-Selective Agonists to Combat Cardiovascular Inflammation.Journal of cardiovascular development and disease · 2017Review
- Differential impact of acute and prolonged cAMP agonist exposure on protein kinase A activation and human myometrium contractile activity.The Journal of physiology · 2016Article
- A-kinase-anchoring proteins coordinate inflammatory responses to cigarette smoke in airway smooth muscle.American journal of physiology. Lung cellular and molecular physiology · 2015Article
- A-kinase anchoring proteins: cAMP compartmentalization in neurodegenerative and obstructive pulmonary diseases.British journal of pharmacology · 2014Review
- β-Agonist-mediated relaxation of airway smooth muscle is protein kinase A-dependent.The Journal of biological chemistry · 2014Article
- Clonally expanded human airway smooth muscle cells exhibit morphological and functional heterogeneity.Respiratory research · 2014Article
- The cAMP effector EPAC activates Elk1 transcription factor in prostate smooth muscle, and is a minor regulator of α1-adrenergic contraction.Journal of biomedical science · 2013Article
- cAMP regulation of airway smooth muscle function.Pulmonary pharmacology & therapeutics · 2013Review
- The β2-subtype of adrenoceptors mediates inhibition of pro-fibrotic events in human lung fibroblasts.Naunyn-Schmiedeberg's archives of pharmacology · 2011Article
- Real time analysis of β(2)-adrenoceptor-mediated signaling kinetics in human primary airway smooth muscle cells reveals both ligand and dose dependent differences.Respiratory research · 2011Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
background and purposePlatelet-derived growth factor (PDGF) modulates the airway smooth muscle (ASM) 'contractile' phenotype to a more 'proliferative' phenotype, resulting in increased proliferation and reduced contractility. Such phenotypic modulation may contribute to airway remodelling in asthma. We have previously shown that the cAMP effector molecules, protein kinase A (PKA) and the exchange protein directly activated by cAMP (Epac) inhibited PDGF-induced phenotypic modulation in bovine ASM. Here, we investigated these mechanisms in human ASM strips and cells. EXPERIMENTAL APPROACH: ASM strips were incubated with PDGF in the absence or presence of the activators of Epac (8-pCPT-2'-O-Me-cAMP) or of PKA (6-Bnz-cAMP) for 4 days. Strips were mounted for isometric contraction experiments or analysed for the expression of contractile markers. Cell proliferation was measured and proliferative markers were analysed under similar conditions. KEY
resultsActivation of Epac and PKA prevented PDGF-induced ASM strip hypocontractility, and restored the expression of smooth muscle actin, myosin and calponin, which had been markedly diminished by PDGF. Epac and PKA activation inhibited the PDGF-induced ASM cell proliferation and G(1)/S phase transition and the expression and phosphorylation of cell cycle regulators. CONCLUSIONS AND IMPLICATIONS: Epac and PKA maintain a normally contractile ASM phenotype in a mitogenic environment, suggesting that specific activators of Epac and PKA may be beneficial in the treatment of airway remodelling in asthma.
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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.