ArticleCellular signalling2016
Sustained exposure to catecholamines affects cAMP/PKA compartmentalised signalling in adult rat ventricular myocytes.
Article in Cellular signalling, 2016. 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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Who cites it
15 citing papers in PubMed, 27 citations in OpenAlex.
- β-Adrenergic Receptor Trafficking, Degradation, and Cell Surface Expression Are Altered in Dermal Fibroblasts from Hypertrophic Scars.The Journal of investigative dermatology · 2018Trial
- Loss of caveolar A1 adenosine receptor signalling blunts anti-adrenergic control in heart failure.Cardiovascular research · 2026Article
- Phospholipase C epsilon 1 as a therapeutic target in cardiovascular diseases.Journal of advanced research · 2025Review
- New Insights in the Diagnostic Potential of Sex Hormone-Binding Globulin (SHBG)-Clinical Approach.Biomedicines · 2025Review
- Nanodomain cAMP signaling in cardiac pathophysiology: potential for developing targeted therapeutic interventions.Physiological reviews · 2025Review
- Review
- AKAP12 Upregulation Associates With PDE8A to Accelerate Cardiac Dysfunction.Circulation research · 2024Article
- Physiological and pathological roles of protein kinase A in the heart.Cardiovascular research · 2022Review
- Classic and Novel Sex Hormone Binding Globulin Effects on the Cardiovascular System in Men.International journal of endocrinology · 2021Review
- Subcellular Organization of the cAMP Signaling Pathway.Pharmacological reviews · 2021Review
- Transcriptomic Validation of the Protective Effects of Aqueous Bark Extract ofFrontiers in pharmacology · 2019Article
- Illuminating cell signaling with genetically encoded FRET biosensors in adult mouse cardiomyocytes.The Journal of general physiology · 2018Article
- Compartmentalized cyclic nucleotides have opposing effects on regulation of hypertrophic phospholipase Cε signaling in cardiac myocytes.Journal of molecular and cellular cardiology · 2018Article
- Cardiac Phosphodiesterases and Their Modulation for Treating Heart Disease.Handbook of experimental pharmacology · 2017Review
- Response to Wagner et al.: phosphodiesterase-2-anti-adrenergic friend or hypertrophic foe in heart disease?Naunyn-Schmiedeberg's archives of pharmacology · 2016Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
In the heart compartmentalisation of cAMP/protein kinase A (PKA) signalling is necessary to achieve a specific functional outcome in response to different hormonal stimuli. Chronic exposure to catecholamines is known to be detrimental to the heart and disrupted compartmentalisation of cAMP signalling has been associated to heart disease. However, in most cases it remains unclear whether altered local cAMP signalling is an adaptive response, a consequence of the disease or whether it contributes to the pathogenetic process. We have previously demonstrated that isoforms of PKA expressed in cardiac myocytes, PKA-I and PKA-II, localise to different subcellular compartments and are selectively activated by spatially confined pools of cAMP, resulting in phosphorylation of distinct downstream targets. Here we investigate cAMP signalling in an in vitro model of hypertrophy in primary adult rat ventricular myocytes. By using a real time imaging approach and targeted reporters we find that that sustained exposure to catecholamines can directly affect cAMP/PKA compartmentalisation. This appears to involve a complex mechanism including both changes in the subcellular localisation of individual phosphodiesterase (PDE) isoforms as well as the relocalisation of PKA isoforms. As a result, the preferential coupling of PKA subsets with different PDEs is altered resulting in a significant difference in the level of cAMP the kinase is exposed to, with potential impact on phosphorylation of downstream targets.
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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.