Cited by 127Retinal Diseases and TreatmentsRetinal Development and DisordersRetinal Imaging and Analysis

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Antioxidant or neurotrophic factor treatment preserves function in a mouse model of neovascularization-associated oxidative stress

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Dorrell, Michael I., Aguilar, Edith, Jacobson, Ruth, Yanes, Oscar, Gariano, Ray, Heckenlively, John, Banin, Eyal, Ramirez, G. Anthony, Gasmi, Mehdi, Bird, Alan, Siuzdak, Gary, Friedlander, Martin·2009·Journal of Clinical Investigation

DOI 10.1172/jci35977PMC PMC2648679

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Abstract

In several disease states, abnormal growth of blood vessels is associated with local neuronal degeneration. This is particularly true in ocular diseases such as retinal angiomatous proliferation (RAP) and macular telangiectasia (MacTel), in which, despite the absence of large-scale leakage or hemorrhage, abnormal neovascularization (NV) is associated with local neuronal dysfunction. We describe here a retinal phenotype in mice with dysfunctional receptors for VLDL (Vldlr-/- mice) that closely resembles human retinal diseases in which abnormal intra- and subretinal NV is associated with photoreceptor cell death. Such cell death was evidenced by decreased cone and, to a lesser extent, rod opsin expression and abnormal electroretinograms. Cell death in the region of intraretinal vascular abnormalities was associated with an increased presence of markers associated with oxidative stress. Oral antioxidant supplementation protected against photoreceptor degeneration and preserved retinal function, despite the continued presence of abnormal intra- and subretinal vessels. What we believe to be novel, Müller cell-based, virally mediated delivery of neurotrophic compounds specifically to sites of NV was also neuroprotective. These observations demonstrate that neuronal loss secondary to NV can be prevented by the use of simple antioxidant dietary measures or cell-based delivery of neurotrophic factors, even when the underlying vascular phenotype is not altered.

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Authors: Dorrell, M. I., Aguilar, E., Jacobson, R., Yanes, O., Gariano, R., Heckenlively, J., Banin, E., Ramirez, G. A., Gasmi, M., Bird, A., Siuzdak, G., & Friedlander, M.
Affiliations: Scripps Research Institute (US)
University of Michigan (US)
Hadassah Medical Center (IL)
Moorfields Eye Hospital (GB)
Corresponding author: Friedlander, Martin
ORCID: Dorrell, Michael I.
Aguilar, Edith
Banin, Eyal
Bird, Alan
Siuzdak, Gary
Friedlander, Martin
Venue: Journal of Clinical Investigation
Publisher: American Society for Clinical Investigation
Published: 2009-03-02
Volume: 119
Issue: 3
Pages: 611-623
ISSN: 0021-9738 (ISSN-L)
DOI: 10.1172/jci35977
PMC: PMC2648679
OpenAlex: W1999304307
Cited by: 127
References: 57
Citations by year: 2026: 4 · 2025: 4 · 2024: 5 · 2023: 3 · 2022: 9 · 2021: 5 · 2020: 8 · 2019: 2 · 2018: 6 · 2017: 15 · 2016: 4 · 2015: 9 · 2014: 7 · 2013: 9 · 2012: 15
FWCI: 12.53
Type: journal article
Language: en
Open access: bronze
doi.org
Locations: Journal of Clinical Investigation (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: California Institute for Regenerative Medicine
V. Kann Rasmussen Foundation
National Institutes of Health
National Eye Institute (R01EY011254)
Topics: Health Sciences › Medicine › Ophthalmology › Retinal Diseases and Treatments
Health Sciences › Medicine › Ophthalmology › Retinal Development and Disorders
Health Sciences › Medicine › Radiology, Nuclear Medicine and Imaging › Retinal Imaging and Analysis
Keywords: neovascularization, oxidative stress, photoreceptor degeneration, retinal angiomatous proliferation, macular telangiectasia, VLDL receptor, antioxidant supplementation, neurotrophic factor delivery, Müller cells, viral gene delivery, retinal function, cone opsin, rod opsin, electroretinogram
MeSH terms: Animals, Antioxidants, Disease Models, Animal, Electroretinography, Mice, Inbred C57BL, Nerve Growth Factors, Receptors, LDL, Retina, Retinitis Pigmentosa, Rhodopsin, Lipid Peroxidation, Retinal Neovascularization, Gene Expression, Retinal Rod Photoreceptor Cells, Retinal Cone Photoreceptor Cells, Gene Transfer Techniques, Mice, Knockout, Oxidative Stress, Angiogenesis Inhibitors, Gene Expression Profiling, Vascular Endothelial Growth Factor A, Mice, Aptamers, Nucleotide, Retinal Pigment Epithelium, Opsins

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Antioxidant or neurotrophic factor treatment preserves function in a mouse model of neovascularization-associated oxidative stress

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