ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2000
Increased production of tumor necrosis factor-alpha by glial cells exposed to simulated ischemia or elevated hydrostatic pressure induces apoptosis in cocultured retinal ganglion cells.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 179 papers, 1 of them a synthesis that pooled it.
What it found
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Who cites it
179 citing papers in PubMed, 1 synthesis or guideline pooled it, 397 citations in OpenAlex.
- Roles of tumor necrosis factor alpha gene polymorphisms, tumor necrosis factor alpha level in aqueous humor, and the risks of open angle glaucoma: a meta-analysis.Molecular vision · 2013Pooled it
- Dual role of microglia in glaucoma: Regulation of neuroinflammation and neuroregeneration.Neural regeneration research · 2026Article
- Spatiotemporal Immune Dynamics in Experimental Retinal Ganglion Cell Injury Models.Immunity, inflammation and disease · 2025Review
- Stroke-Induced Retinal Dysfunction: Mechanisms, Diagnostics, and Future Directions.Aging and disease · 2025Review
- Mapping key trends, relationships, and molecular pathways for neuroprotection in glaucoma: a bibliometric approach.International journal of ophthalmology · 2025Article
- Retinal transplant immunology and advancements.Stem cell reports · 2024Review
- cFLIP in the molecular regulation of astroglia-driven neuroinflammation in experimental glaucoma.Journal of neuroinflammation · 2024Article
- Glaucoma: from pathogenic mechanisms to retinal glial cell response to damage.Frontiers in cellular neuroscience · 2024Review
- Oxidative stress in the eye and its role in the pathophysiology of ocular diseases.Redox biology · 2023Review
- Therapeutic Potential of Antioxidants and Hybrid TEMPOL Derivatives in Ocular Neurodegenerative Diseases: A Glimpse into the Future.Biomedicines · 2023Review
- Molecular mechanisms of NMDA excitotoxicity in the retina.Scientific reports · 2023Article
- Immunomodulatory and Antioxidant Drugs in Glaucoma Treatment.Pharmaceuticals (Basel, Switzerland) · 2023Review
- Oxidative Stress: A Suitable Therapeutic Target for Optic Nerve Diseases?Antioxidants (Basel, Switzerland) · 2023Review
- L- and T-type CaNeural regeneration research · 2023Article
- Role of A-Kinase Anchoring Protein 1 in Retinal Ganglion Cells: Neurodegeneration and Neuroprotection.Cells · 2023Review
- Fluoxetine Protects Retinal Ischemic Damage in Mice.Pharmaceutics · 2023Article
- Aqueous humor cytokine levels are associated with the severity of visual field defects in patients with primary open-angle glaucoma.BMC ophthalmology · 2023Article
- Factors Associated with Elevated Tumor Necrosis Factor-α in Aqueous Humor of Patients with Open-Angle Glaucoma.Journal of clinical medicine · 2022Article
- Retinal Ganglion Cell Survival and Axon Regeneration after Optic Nerve Injury: Role of Inflammation and Other Factors.International journal of molecular sciences · 2022Review
- Article
119 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
Although glial cells in the optic nerve head undergo a reactivation process in glaucoma, the role of glial cells during glaucomatous neurodegeneration of retinal ganglion cells is unknown. Using a coculture system in which retinal ganglion cells and glial cells are grown on different layers but share the same culture medium, we studied the influences of glial cells on survival of retinal ganglion cells after exposure to different stress conditions typified by simulated ischemia and elevated hydrostatic pressure. After the exposure to these stressors, we observed that glial cells secreted tumor necrosis factor-alpha (TNF-alpha) as well as other noxious agents such as nitric oxide into the coculture media and facilitated the apoptotic death of retinal ganglion cells as assessed by morphology, terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling, and caspase activity. The glial origin of these noxious effects was confirmed by passive transfer experiments. Furthermore, retinal ganglion cell apoptosis was attenuated approximately 66% by a neutralizing antibody against TNF-alpha and 50% by a selective inhibitor of inducible nitric oxide synthase (1400W). Because elevated intraocular pressure and ischemia are two prominent stress factors identified in the eyes of patients with glaucoma, these findings reveal a novel glia-initiated pathogenic mechanism for retinal ganglion cell death in glaucoma. In addition, these findings suggest that the inhibition of TNF-alpha that is released by reactivated glial cells may provide a novel therapeutic target for neuroprotection in the treatment of glaucomatous optic neuropathy.
Indexed as
Identifiers
11102475PMC6773089W1624269173What OpenQuestion holds
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.