ArticleJournal of neuroinflammation2015
Adenosine A2AR blockade prevents neuroinflammation-induced death of retinal ganglion cells caused by elevated pressure.
Article in Journal of neuroinflammation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 82 citations in OpenAlex.
- Article
- Adenosine A2A receptor signaling in neuroinflammation, glial modulation, and mechanisms associated with chronic pain.Purinergic signalling · 2026Review
- Adenosine A2a receptors offset cholinergic control of blood pressure, autonomic neuropathy, and brainstem neuroinflammation in sepsis.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- 40 Hz flicker preconditioning protects nonarteritic anterior ischemic optic neuropathy via adenosine signaling.Communications biology · 2026Article
- Advancing In Vitro Microfluidic Models for Pressure-Induced Retinal Ganglion Cell Degeneration: Current Insights and Future Directions from a Biomechanical Perspective.Micromachines · 2025Article
- Functional significance of commonly regulated genes in mechanically and chemically induced retinal ganglion cell death in rat eyes.Scientific reports · 2025Article
- Cannabinoids as Multitarget Drugs for the Treatment of Autoimmunity in Glaucoma.ACS pharmacology & translational science · 2025Review
- Challenging glaucoma with emerging therapies: an overview of advancements against the silent thief of sight.Frontiers in medicine · 2025Review
- Bioactive Glial-Derived Neurotrophic Factor from a Safe Injectable Collagen-Alginate Composite Gel Rescues Retinal Photoreceptors from Retinal Degeneration in Rabbits.Marine drugs · 2024Article
- Apoptosis in glaucoma: A new direction for the treatment of glaucoma (Review).Molecular medicine reports · 2024Review
- Comparative Analysis of Retinal Organotypic Cultures and In Vivo Axotomized Retinas.International journal of molecular sciences · 2023Article
- Effect of caffeine on genes expressions of developing retinas in the chick model.Anatomy & cell biology · 2022Article
- Impact of Caffeine on Alzheimer's Disease Pathogenesis-Protective or Risk Factor?Life (Basel, Switzerland) · 2022Review
- The adenosine AFrontiers in pharmacology · 2022Article
- Microglial exosomes in retinal neuroinflammation: focus in glaucoma.Neural regeneration research · 2021Article
- Review
- Review
- Adenosine receptors as promising targets for the management of ocular diseases.Medicinal chemistry research : an international journal for rapid communications on design and mechanisms of action of biologically active agents · 2021Review
- The Effect of Plasma Rich in Growth Factors on Microglial Migration, Macroglial Gliosis and Proliferation, and Neuronal Survival.Frontiers in pharmacology · 2021Article
- Adenosine AFrontiers in neuroscience · 2021Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundElevated intraocular pressure (IOP) is a major risk factor for glaucoma, a degenerative disease characterized by the loss of retinal ganglion cells (RGCs). There is clinical and experimental evidence that neuroinflammation is involved in the pathogenesis of glaucoma. Since the blockade of adenosine A2A receptor (A2AR) confers robust neuroprotection and controls microglia reactivity in the brain, we now investigated the ability of A2AR blockade to control the reactivity of microglia and neuroinflammation as well as RGC loss in retinal organotypic cultures exposed to elevated hydrostatic pressure (EHP) or lipopolysaccharide (LPS).
methodsRetinal organotypic cultures were either incubated with LPS (3 μg/mL), to elicit a pro-inflammatory response, or exposed to EHP (+70 mmHg), to mimic increased IOP, for 4 or 24 h, in the presence or absence of the A2AR antagonist SCH 58261 (50 nM). A2AR expression, microglial reactivity and neuroinflammatory response were evaluated by immunohistochemistry, quantitative PCR (qPCR) and enzyme-linked immunosorbent assay (ELISA). RGC loss was assessed by immunohistochemistry. In order to investigate the contribution of pro-inflammatory mediators to RGC loss, the organotypic retinal cultures were incubated with rabbit anti-tumour necrosis factor (TNF) (2 μg/mL) and goat anti-interleukin-1β (IL-1β) (1 μg/mL) antibodies.
resultsWe report that the A2AR antagonist (SCH 58261) prevented microglia reactivity, increase in pro-inflammatory mediators as well as RGC loss upon exposure to either LPS or EHP. Additionally, neutralization of TNF and IL-1β prevented RGC loss induced by LPS or EHP.
conclusionsThis work demonstrates that A2AR blockade confers neuroprotection to RGCs by controlling microglia-mediated retinal neuroinflammation and prompts the hypothesis that A2AR antagonists may be a novel therapeutic option to manage glaucomatous disorders.
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