ArticleJournal of neuroinflammation2016
Bilateral neuroinflammatory processes in visual pathways induced by unilateral ocular hypertension in the rat.
Article in Journal of neuroinflammation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 69 citations in OpenAlex.
- Citicoline and Coenzyme Q10: Therapeutic Agents for Glial Activation Reduction in Ocular Hypertension.Pharmaceuticals (Basel, Switzerland) · 2025Article
- TRPA1 exacerbates selective retinal ganglion cell vulnerability under acute ocular hypertension.Acta neuropathologica communications · 2025Article
- Optic Nerve Crush Does Not Induce Retinal Ganglion Cell Loss in the Contralateral Eye.Investigative ophthalmology & visual science · 2025Article
- Neuroprotective Effect of the Combination of Citicoline and CoQ10 in a Mouse Model of Ocular Hypertension.Antioxidants (Basel, Switzerland) · 2024Article
- Evaluation of Rho kinase inhibitor effects on neuroprotection and neuroinflammation in an ex-vivo retinal explant model.Acta neuropathologica communications · 2024Article
- Pathological high intraocular pressure induces glial cell reactive proliferation contributing to neuroinflammation of the blood-retinal barrier via the NOX2/ET-1 axis-controlled ERK1/2 pathway.Journal of neuroinflammation · 2024Article
- Immune Analysis Using Vitreous Optical Coherence Tomography Imaging in Rats with Steroid-Induced Glaucoma.Biomedicines · 2024Article
- Review
- In a novel autoimmune and high-pressure glaucoma model a complex immune response is induced.Frontiers in immunology · 2024Article
- Chronic Glaucoma Induced in Rats by a Single Injection of Fibronectin-Loaded PLGA Microspheres: IOP-Dependent and IOP-Independent Neurodegeneration.International journal of molecular sciences · 2023Article
- Mitochondrial Open Reading Frame of the 12S rRNA Type-c: Potential Therapeutic Candidate in Retinal Diseases.Antioxidants (Basel, Switzerland) · 2023Review
- Mimicking chronic glaucoma over 6 months with a single intracameral injection of dexamethasone/fibronectin-loaded PLGA microspheres.Drug delivery · 2022Article
- Tunable degrees of neurodegeneration in rats based on microsphere-induced models of chronic glaucoma.Scientific reports · 2022Article
- Apolipoprotein E4 impairs the response of neurodegenerative retinal microglia and prevents neuronal loss in glaucoma.Immunity · 2022Article
- Histological and Top-Down Proteomic Analyses of the Visual Pathway in the Cuprizone Demyelination Model.Journal of molecular neuroscience : MN · 2022Article
- Molecular regulation of neuroinflammation in glaucoma: Current knowledge and the ongoing search for new treatment targets.Progress in retinal and eye research · 2022Review
- Role of Oxidative Stress in Retinal Disease and the Early Intervention Strategies: A Review.Oxidative medicine and cellular longevity · 2022Review
- The heterogeneity of astrocytes in glaucoma.Frontiers in neuroanatomy · 2022Review
- Degeneration of retina-brain components and connections in glaucoma: Disease causation and treatment options for eyesight preservation.Current research in neurobiology · 2022Review
- Interplay between Müller cells and microglia aggravates retinal inflammatory response in experimental glaucoma.Journal of neuroinflammation · 2021Article
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGlaucoma is one of the leading causes of irreversible blindness in the world. The major risk factor is elevated intraocular pressure (IOP) leading to progressive retinal ganglion cell (RGC) death from the optic nerve (ON) to visual pathways in the brain. Glaucoma has been reported to share mechanisms with neurodegenerative disorders. We therefore hypothesize that neuroinflammatory mechanisms in central visual pathways may contribute to the spread of glaucoma disease. The aim of the present study was to analyze the neuroinflammation processes that occur from the pathological retina to the superior colliculi (SCs) in a rat model of unilateral ocular hypertension induced by episcleral vein cauterization (EVC).
resultsSix weeks after unilateral (right eye) EVC in male Long-Evans rats, we evaluated both the neurodegenerative process and the neuroinflammatory state in visual pathway tissues. RGCs immunolabeled (Brn3a(+)) in ipsilateral whole flat-mounted retina demonstrated peripheral RGC loss associated with tissue macrophage/microglia activation (CD68(+)). Gene expression analysis of hypertensive and normotensive retinas revealed a significant increase of pro-inflammatory genes such as CCL2, IL-1β, and Nox2 mRNA expression compared to naïve eyes. Importantly, we found an upregulation of pro-inflammatory markers such as IL-1β and TNFα and astrocyte and tissue macrophage/microglia activation in hypertensive and normotensive RGC projection sites in the SCs compared to a naïve SC. To understand how neuroinflammation in the hypertensive retina is sufficient to damage both right and left SCs and the normotensive retina, we used an inflammatory model consisting in an unilateral stereotaxic injection of TNFα (25 ng/μl) in the right SC of naïve rats. Two weeks after TNFα injection, using an optomotor test, we observed that rats had visual deficiency in both eyes. Furthermore, both SCs showed an upregulation of genes and proteins for astrocytes, microglia, and pro-inflammatory cytokines, notably IL-1β. In addition, both retinas exhibited a significant increase of inflammatory markers compared to a naïve retina.
conclusionsAll these data evidence the complex role played by the SCs in the propagation of neuroinflammatory events induced by unilateral ocular hypertension and provide a new insight into the spread of neurodegenerative diseases such as glaucoma.
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