ArticleBritish journal of pharmacology2011
A2B adenosine receptors inhibit superoxide production from mitochondrial complex I in rabbit cardiomyocytes via a mechanism sensitive to Pertussis toxin.
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 20 papers.
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Who cites it
20 citing papers in PubMed, 39 citations in OpenAlex.
- Therapeutic potential of adenosine receptor modulators in cancer treatment.RSC advances · 2025Review
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- APurinergic signalling · 2025Review
- A2B adenosine receptor-triggered intracellular calcium mobilization: Cell type-dependent involvement of Gi, Gq, Gs proteins and protein kinase C.Research square · 2024Article
- Current Understanding of the Role of Adenosine Receptors in Cancer.Molecules (Basel, Switzerland) · 2024Review
- Article
- Species dependence of APurinergic signalling · 2023Review
- AiScience · 2023Article
- Mitochondrial ROS production by neutrophils is required for host antimicrobial function against Streptococcus pneumoniae and is controlled by A2B adenosine receptor signaling.PLoS pathogens · 2022Article
- Agonist-Dependent Coupling of the Promiscuous Adenosine AACS pharmacology & translational science · 2022Article
- Activation of the adenosine A2B receptor even beyond the therapeutic window of N-acetylcysteine accelerates liver recovery after an acetaminophen overdose.Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association · 2022Article
- Structure and function of adenosine receptor heteromers.Cellular and molecular life sciences : CMLS · 2021Review
- Pharmacological Tuning of Adenosine Signal Nuances Underlying Heart Failure With Preserved Ejection Fraction.Frontiers in pharmacology · 2021Review
- 5-N-ethyl Carboxamidoadenosine Stimulates Adenosine-2b Receptor-Mediated Mitogen-Activated Protein Kinase Pathway to Improve Brain Mitochondrial Function in Amyloid Beta-Induced Cognitive Deficit Mice.Neuromolecular medicine · 2020Article
- On the G protein-coupling selectivity of the native ABiochemical pharmacology · 2018Article
- Differential Tissue-Specific Function of Adora2b in Cardioprotection.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- Probing biased/partial agonism at the G protein-coupled A(2B) adenosine receptor.Biochemical pharmacology · 2014Article
- Evidence for the involvement of NADPH oxidase in adenosine receptors-mediated control of coronary flow using APhysiological reports · 2013Article
- All preconditioning-related G protein-coupled receptors can be demonstrated in the rabbit cardiomyocyte.Journal of cardiovascular pharmacology and therapeutics · 2012Article
- Transgenic over expression of ectonucleotide triphosphate diphosphohydrolase-1 protects against murine myocardial ischemic injury.Journal of molecular and cellular cardiology · 2011Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
background and purposeA(2B) adenosine receptors protect against ischaemia/reperfusion injury by activating survival kinases including extracellular signal-regulated kinase (ERK) and phosphatidylinositol 3-kinase (PI3K). However, the underlying mechanism(s) and signalling pathway(s) remain undefined. EXPERIMENTAL APPROACH: HEK 293 cells stably transfected with human A(2B) adenosine receptors (HEK-A(2B) ) and isolated adult rabbit cardiomyocytes were used to assay phosphorylation of ERK by Western blot and cation flux through cAMP-gated channels by patch clamp methods. Generation of reactive oxygen species (ROS) by mitochondria was measured with a fluorescent dye. KEY
resultsIn HEK-A(2B) cells, the selective A(2B) receptor agonist Bay 60-6583 (Bay 60) increased ERK phosphorylation and cAMP levels, detected by current through cAMP-gated ion channels. However, increased cAMP or its downstream target protein kinase A was not involved in ERK phosphorylation. Pertussis toxin (PTX) blocked ERK phosphorylation, suggesting receptor coupling to G(i) or G(o) proteins. Phosphorylation was also blocked by inhibition of PI3K (with wortmannin) or of ERK kinase (MEK1/2, with PD 98059) but not by inhibition of NO synthase (NOS). In cardiomyocytes, Bay 60 did not affect cAMP levels but did block the increased superoxide generation induced by rotenone, a mitochondrial complex I inhibitor. This effect of Bay 60 was inhibited by PD 98059, wortmannin or PTX. Inhibition of NOS blocked superoxide production because NOS is downstream of ERK. CONCLUSION AND IMPLICATIONS: Activation of A(2B) adenosine receptors reduced superoxide generation from mitochondrial complex I through G(i/o) , ERK, PI3K, and NOS, all of which have been implicated in ischaemic preconditioning.
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