ArticleAmerican journal of physiology. Lung cellular and molecular physiology2015
A-kinase-anchoring proteins coordinate inflammatory responses to cigarette smoke in airway smooth muscle.
Article in American journal of physiology. Lung cellular and molecular physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 29 citations in OpenAlex.
- A-Kinase-Anchoring Protein Subtypes Differentially Regulate GPCR Signaling and Function in Human Airway Smooth Muscle.American journal of respiratory cell and molecular biology · 2025Article
- Article
- Diesel exhaust particles alter mitochondrial bioenergetics and cAMP producing capacity in human bronchial epithelial cells.Frontiers in toxicology · 2024Article
- Loss of AKAP12 aggravates rheumatoid arthritis-like symptoms and cardiac damage in collagen-induced arthritis mice.Experimental animals · 2023Article
- Synaptic retrograde regulation of the PKA-induced SNAP-25 and Synapsin-1 phosphorylation.Cellular & molecular biology letters · 2023Article
- AKAP12/Gravin is over-expressed in patients with ulcerative colitis.Immunologic research · 2021Article
- Cigarette smoke-induced alterations in blood: A review of research on DNA methylation and gene expression.Experimental and clinical psychopharmacology · 2021Review
- Article
- A-Kinase Anchoring Proteins Diminish TGF-βCells · 2020Article
- Low expression of A-kinase anchor protein 5 predicts poor prognosis in non-mucin producing stomach adenocarcinoma based on TCGA data.Annals of translational medicine · 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
- Function of cAMP scaffolds in obstructive lung disease: Focus on epithelial-to-mesenchymal transition and oxidative stress.British journal of pharmacology · 2019Review
- Cigarette smoke up-regulates PDE3 and PDE4 to decrease cAMP in airway cells.British journal of pharmacology · 2018Article
- Epac Function and cAMP Scaffolds in the Heart and Lung.Journal of cardiovascular development and disease · 2018Review
- Deduction of Novel Genes Potentially Involved in Osteoblasts of Rheumatoid Arthritis Using Next-Generation Sequencing and Bioinformatic Approaches.International journal of molecular sciences · 2017Article
- Loss of AKAP150 promotes pathological remodelling and heart failure propensity by disrupting calcium cycling and contractile reserve.Cardiovascular research · 2017Article
- The novel compound Sul-121 inhibits airway inflammation and hyperresponsiveness in experimental models of chronic obstructive pulmonary disease.Scientific reports · 2016Article
- Scaffolding during the cell cycle by A-kinase anchoring proteins.Pflugers Archiv : European journal of physiology · 2015Review
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Authors and funding
9 authors at 4 institutions in 4 countries.
Funding
Abstract
β2-Agonist inhibitors can relieve chronic obstructive pulmonary disease (COPD) symptoms by stimulating cyclic AMP (cAMP) signaling. A-kinase-anchoring proteins (AKAPs) compartmentalize cAMP signaling by establishing protein complexes. We previously reported that the β2-agonist fenoterol, direct activation of protein kinase A (PKA), and exchange factor directly activated by cAMP decrease cigarette smoke extract (CSE)-induced release of neutrophil attractant interleukin-8 (IL-8) from human airway smooth muscle (ASM) cells. In the present study, we tested the role of AKAPs in CSE-induced IL-8 release from ASM cells and assessed the effect of CSE on the expression levels of different AKAPs. We also studied mRNA and protein expression of AKAPs in lung tissue from patients with COPD. Our data show that CSE exposure of ASM cells decreases AKAP5 and AKAP12, both capable of interacting with β2-adrenoceptors. In lung tissue of patients with COPD, mRNA levels of AKAP5 and AKAP12 were decreased compared with lung tissue from controls. Using immunohistochemistry, we detected less AKAP5 protein in ASM of patients with COPD Global Initiative for Chronic Obstructive Lung Disease (GOLD) stage II compared with control subjects. St-Ht31, which disrupts AKAP-PKA interactions, augmented CSE-induced IL-8 release from ASM cells and diminished its suppression by fenoterol, an effect mediated by disturbed ERK signaling. The modulatory role of AKAP-PKA interactions in the anti-inflammatory effects of fenoterol in ASM cells and the decrease in expression of AKAP5 and AKAP12 in response to cigarette smoke and in lungs of patients with COPD suggest that cigarette smoke-induced changes in AKAP5 and AKAP12 in patients with COPD may affect efficacy of pharmacotherapy.
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Registered trials
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