Murine Ccl2/Cx3cr1 Deficiency Results in Retinal Lesions Mimicking Human Age-Related Macular Degeneration
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PURPOSE: Senescent Ccl2(-/-) mice are reported to develop cardinal features of human age-related macular degeneration (AMD). Loss-of-function single-nucleotide polymorphisms within CX3CR1 are also found to be associated with AMD. The authors generated Ccl2(-/-)/Cx3cr1(-/-) mice to establish a more characteristic and reproducible AMD model. METHODS: Single Ccl2- and Cx3cr1-deficient mice were crossbred to obtain Ccl2(-/-)/Cx3cr1(-/-) mice. Funduscopy, histopathology, retinal A2E quantification, proteomics, RT-PCR gene expression assay, immunochemistry, and Western blotting were used to examine the retina and to evaluate gene expression within the retinal tissue. RESULTS: By 6 weeks of age, all Ccl2(-/-)/Cx3cr1(-/-) mice developed AMD-like retinal lesions, including drusen, retinal pigment epithelium alteration, and photoreceptor degeneration. Furthermore, choroidal neovascularization occurred in 15% of the mice. These degenerative lesions progressed with age. A2E, a major lipofuscin fluorophore that accumulated during AMD progression, was significantly higher in the Ccl2(-/-)/Cx3cr1(-/-) retina than in the wild-type retina. Complement cofactor was higher in the Ccl2(-/-)/Cx3cr1(-/-) RPE. Proteomics data indicated that four proteins were differentially expressed in Ccl2(-/-)/Cx3cr1(-/-) retina compared with control. One of these proteins, ERp29, an endoplasmic reticulum protein, functions as an escort chaperone and in protein folding. CONCLUSIONS: The authors concluded that Ccl2(-/-)/Cx3cr1(-/-) mice develop a broad spectrum of AMD abnormalities with early onset and high penetrance. These observations implicate certain chemokines and endoplasmic reticulum proteins in AMD pathogenesis. Similar to the mechanism of neurodegeneration caused by dysfunction of endoplasmic reticulum proteins, decreased chaperoning may cause misfolded protein accumulation, leading to drusen formation and retinal degeneration.
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Ccl2/Cx3cr1 double knockout mice show ultrastructural AMD signs including lipofuscin granule accumulation and increased A2E accumulation on biochemical analysis.
“These mice also exhibited ultrastructural signs of AMD such as accumulation of lipofuscin granules, as well as increased the N-retinylidene–N-retinylethanolamine (A2E) accumulation on biochemical analysis (Chan et al., 2008; Tuo et al., 2007).”
From Molecular pathology of age-related macular degeneration (2009) · cites this paper as Tuo et al., 2007
Ccl2/Cx3cr1 double knockout mice exhibit fundoscopically visible drusen-like lesions at 4-6 weeks of age, histological AMD signs including Bruch's membrane thickening, drusen, local RPE hypopigmentation and degeneration, photoreceptor disorganization and atrophy, and CNV in some mice.
“We found that Ccl2−/−/Cx3cr1−/− mice exhibited, at an early age of 4–6 weeks, fundoscopically visible drusen-like lesions, as well as histological signs of AMD such as thickening of Bruch’s membrane, drusen, local RPE hypopigmentation and degeneration, and photoreceptor disorganization and atrophy, as well as CNV in some mice.”
From Molecular pathology of age-related macular degeneration (2009) · cites this paper as Tuo et al., 2007
Spontaneous CNV was present in about 15% of Ccl2−/−/Cx3cr1−/− mice.
“Spontaneous CNV was present in about 15% of Ccl2−/−/Cx3cr1−/− mice (Tuo et al., 2007).”
From Retinal ultrastructure of murine models of dry age-related macular degeneration (AMD) (2010) · cites this paper as Tuo et al., 2007
Ccl2−/−/Cx3cr1−/− mice began exhibiting drusen-like lesions on fundoscopy as early as 4-6 weeks of age.
“Ccl2−/−/Cx3cr1−/− mice began exhibiting drusen-like lesions on fundoscopy as early as 4–6 weeks of age.”
From Retinal ultrastructure of murine models of dry age-related macular degeneration (AMD) (2010) · cites this paper as Tuo et al., 2007
The Ccl2−/−/Cx3cr1−/− mouse model has demonstrated early onset of the AMD phenotype with high penetrance.
“The Ccl2−/−/Cx3cr1−/− mouse model has demonstrated early onset of the AMD phenotype with high penetrance (Tuo et al., 2007).”
From Retinal ultrastructure of murine models of dry age-related macular degeneration (AMD) (2010) · cites this paper as Tuo et al., 2007
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- Authors
- Tuo, J., Bojanowski, C. M., Zhou, M., Shen, D., Ross, R. J., Rosenberg, K. I., Cameron, D. J., Yin, C., Kowalak, J. A., Zhuang, Z., Zhang, K., & Chan, C.-C.
- Affiliations
- National Institutes of Health (US)
- National Eye Institute (US)
- University of Utah (US)
- National Institute of Neurological Disorders and Stroke (US)
- ORCID
- Venue
- Investigative Opthalmology & Visual Science
- Published
- 2007-08-01
- Volume
- 48
- Issue
- 8
- Pages
- 3827
- ISSN
- 0146-0404 (ISSN-L)
- 1552-5783
- PMC
- PMC2048751
- OpenAlex
- W1969157499
- Cited by
- 205
- References
- 75
- Citations by year
- 2026: 2 · 2025: 2 · 2024: 6 · 2023: 5 · 2022: 6 · 2021: 4 · 2020: 7 · 2019: 5 · 2018: 7 · 2017: 8 · 2016: 9 · 2015: 15 · 2014: 16 · 2013: 17 · 2012: 30
- FWCI
- 16.38
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Investigative Ophthalmology & Visual Science (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Eye Institute (Z01EY000418)
- National Institute of Allergy and Infectious Diseases
- Topics
- Health Sciences › Medicine › Ophthalmology › Retinal Diseases and Treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Retinal Development and Disorders
- Health Sciences › Medicine › Radiology, Nuclear Medicine and Imaging › Retinal Imaging and Analysis
- Keywords
- age-related macular degeneration, MCP-1, CX3CR1, chemokine deficiency, retinal lesions, drusen, retinal pigment epithelium, photoreceptor degeneration, choroidal neovascularization, A2E, lipofuscin, ERp29, endoplasmic reticulum chaperone, protein misfolding, mouse model
- MeSH terms
- CX3C Chemokine Receptor 1, Aging, Animals, Complement C3b, Disease Models, Animal, Endoplasmic Reticulum, Female, Heat-Shock Proteins, Humans, Macular Degeneration, Male, Mice, Inbred C57BL, Pyridinium Compounds, Retina, Retinoids, Retinal Drusen, Complement C4b, Microglia, Mice, Knockout, Chemokine CCL2, Receptors, Chemokine, Microscopy, Electron, Transmission, Mice
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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