ArticleFEBS letters1998
Activation of the A2A adenosine receptor inhibits nitric oxide production in glial cells.
Article in FEBS letters, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
22 citing papers in PubMed, 76 citations in OpenAlex.
- Regulation of Inducible Nitric Oxide Synthase (NOS2) Expression in Healthy and Inflamed Bowel: A Narrative Review.International journal of molecular sciences · 2026Review
- G protein-coupled receptors in neurodegenerative diseases and psychiatric disorders.Signal transduction and targeted therapy · 2023Review
- Comparative assessment of the effects of DREADDs and endogenously expressed GPCRs in hippocampal astrocytes on synaptic activity and memory.Frontiers in cellular neuroscience · 2023Review
- Adenosine as a Key Mediator of Neuronal Survival in Cerebral Ischemic Injury.Neurochemical research · 2022Review
- AβCellular and molecular life sciences : CMLS · 2022Article
- Article
- Squalene-based multidrug nanoparticles for improved mitigation of uncontrolled inflammation in rodents.Science advances · 2020Article
- Inflammation in stroke: the role of cholinergic, purinergic and glutamatergic signaling.Therapeutic advances in neurological disorders · 2018Review
- The purinergic neurotransmitter revisited: a single substance or multiple players?Pharmacology & therapeutics · 2014Review
- Adenosine A2A receptors modulate acute injury and neuroinflammation in brain ischemia.Mediators of inflammation · 2014Review
- Glial adenosine kinase--a neuropathological marker of the epileptic brain.Neurochemistry international · 2013Review
- Neuronal and glial purinergic receptors functions in neuron development and brain disease.Frontiers in cellular neuroscience · 2013Review
- Effects of adenosine receptor antagonists on the in vivo LPS-induced inflammation model of Parkinson's disease.Neurotoxicity research · 2013Article
- Alcohol and risk of Parkinson's disease in a large, prospective cohort of men and women.Movement disorders : official journal of the Movement Disorder Society · 2012Article
- Receptor crosstalk: haloperidol treatment enhances A(2A) adenosine receptor functioning in a transfected cell model.Purinergic signalling · 2010Article
- Adenosine signaling and function in glial cells.Cell death and differentiation · 2010Review
- Pathophysiological roles for purines: adenosine, caffeine and urate.Progress in brain research · 2010Review
- Purinoceptors on neuroglia.Molecular neurobiology · 2009Review
- P1 receptors and cytokine secretion.Purinergic signalling · 2007Article
- Adenosine receptor signaling in the brain immune system.Trends in pharmacological sciences · 2005Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 3 institutions in 2 countries.
Funding
Abstract
Selective adenosine receptor agonists and antagonists have marked effects on the outcome of cerebral ischemia, and adenosine receptors are expressed on astrocytes. In this study we examined the effects of various adenosine receptor agonists on the production of nitric oxide and the induction of iNOS in astrocytes activated by LPS/IFN-gamma and TNF-alpha/IL-1beta and on the production of TNF-alpha. Treatment of the cells with the A2A receptor agonist CGS 21680 inhibited both NO production and iNOS expression induced by stimulation with either LPS/IFN-gamma or TNF-alpha/IL-1beta, whereas the A1 and A3 receptor agonists, CPA and Cl-IB-MECA, respectively, did not have significant inhibitory effects. The inhibitory effect of the A2A receptor agonist was antagonized by the specific A2A receptor antagonist CSC. The A2A agonist also exerted a small inhibitory effect on the production of TNF-alpha. Similar inhibitory effects on the production of NO were obtained by cyclic AMP-elevating reagents, such as forskolin and dibutyryl cyclic AMP. Our findings suggest that activation of the A2A receptor inhibits NO production and iNOS expression likely via increased cAMP.
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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.