ArticleJournal of neuroinflammation2022
A novel aquaporin-4-associated optic neuritis rat model with severe pathological and functional manifestations.
Article in Journal of neuroinflammation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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13 citing papers in PubMed, 16 citations in OpenAlex.
- Dynamic characterization of pathological and functional deterioration in a mouse model of optic neuritis related to neuromyelitis optica spectrum disorder.Neural regeneration research · 2026Article
- Therapeutic effects of IGF-2 on NMOSD by inhibiting astrocyte apoptosis through modulation of the IGF-1R/PI3K/AKT signaling pathway.Scientific reports · 2026Article
- Dissecting NMOSD pathogenesis through animal models: a mechanism-oriented systems perspective.Frontiers in immunology · 2026Review
- Critical analysis of translational potential of rodent models of white matter pathology across a wide spectrum of human diseases.Cell death & disease · 2025Review
- Aquaporin-4 Peptide Injection in Mice Induces Retinal and Optic Nerve Alterations That Simulate Those of Neuromyelitis Optica Spectrum Disorder.Translational vision science & technology · 2025Article
- Non-human primates as preclinical models for optic nerve research: advancing insights into their application and potential.Eye (London, England) · 2025Review
- Intravitreal delivery of NMO-IgG causes primary retinal damage in the absence of optic nerve injury.Journal of neuroinflammation · 2025Article
- The Different Immune Response Between Onset and Remission of AQP4 Antibody-Positive Optic Neuritis Based on RNA Sequencing of Whole Blood.Journal of inflammation research · 2025Article
- Rituximab maintenance treatment outcomes in patients with relapsing neuromyelitis optica spectrum disorder: a monocentric retrospective analysis.Acta neurologica Belgica · 2024Article
- Cobalt Toxicity Induces Retinopathy and Optic Neuropathy in Mice.Investigative ophthalmology & visual science · 2024Article
- Article
- Humanized-Aquaporin-4-Expressing Rat Created by Gene-Editing Technology and Its Use to Clarify the Pathology of Neuromyelitis Optica Spectrum Disorder.International journal of molecular sciences · 2024Article
- Scientific issues with rodent models of neuromyelitis optic spectrum disorders.Frontiers in immunology · 2024Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
backgroundOptic neuritis (ON) is a common manifestation of aquaporin-4 (AQP4) antibody seropositive neuromyelitis optica (NMO). The extent of tissue damage is frequently severe, often leading to loss of visual function, and there is no curative treatment for this condition. To develop a novel therapeutic strategy, elucidating the underlying pathological mechanism using a clinically relevant experimental ON model is necessary. However, previous ON animal models have only resulted in mild lesions with limited functional impairment. In the present study, we attempted to establish a feasible ON model with severe pathological and functional manifestations using a high-affinity anti-AQP4 antibody. Subsequently, we aimed to address whether our model is suitable for potential drug evaluation by testing the effect of minocycline, a well-known microglia/macrophage inhibitor.
methodsAQP4-immunoglobulin G (IgG)-related ON in rats was induced by direct injection of a high-affinity anti-AQP4 monoclonal antibody, E5415A. Thereafter, the pathological and functional characterizations were performed, and the therapeutic potential of minocycline was investigated.
resultsWe established an experimental ON model that reproduces the histological characteristics of ON in seropositive NMO, such as loss of AQP4/glial fibrillary acidic protein immunoreactivity, immune cell infiltration, and extensive axonal damage. We also observed that our rat model exhibited severe visual dysfunction. The histological analysis showed prominent accumulation of macrophages/activated microglia in the lesion site in the acute phase. Thus, we investigated the possible effect of the pharmacological inhibition of macrophages/microglia activation by minocycline and revealed that it effectively ameliorated axonal damage and functional outcome.
conclusionsWe established an AQP4-IgG-induced ON rat model with severe functional impairments that reproduce the histological characteristics of patients with NMO. Using this model, we revealed that minocycline treatment ameliorates functional and pathological outcomes, highlighting the usefulness of our model for evaluating potential therapeutic drugs for ON in NMO.
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