ArticleInvestigative ophthalmology & visual science2015
A chimeric Cfh transgene leads to increased retinal oxidative stress, inflammation, and accumulation of activated subretinal microglia in mice.
Article in Investigative ophthalmology & visual science, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
33 citing papers in PubMed, 35 citations in OpenAlex.
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- TREM2 in age-related macular degeneration: a microglia-centered perspective in the retinal myeloid landscape.Frontiers in ophthalmology · 2026Review
- A mutation inMolecular vision · 2026Article
- Therapeutic potential of P2X7 receptor in retinal diseases.Purinergic signalling · 2025Review
- Isolation and Characterization of Mouse Choroidal Melanocytes and Their Proinflammatory Characteristics.Cells · 2025Article
- Complement factor H in molecular regulation of angiogenesis.Medical review (2021) · 2024Review
- Aberrant Lipid Metabolism and Complement Activation in Age-Related Macular Degeneration.Investigative ophthalmology & visual science · 2024Review
- Modeling complex age-related eye disease.Progress in retinal and eye research · 2024Review
- E3 ubiquitin ligase Herc3 deficiency leads to accumulation of subretinal microglia and retinal neurodegeneration.Scientific reports · 2024Article
- Recent Advances in Our Understanding of Age-Related Macular Degeneration: Mitochondrial Dysfunction, Redox Signaling, and the Complement System.Aging and disease · 2024Review
- The complement system in lipid-mediated pathologies.Frontiers in immunology · 2024Review
- Retinal debris triggers cytotoxic damage in cocultivated primary porcine RPE cells.Frontiers in neuroscience · 2024Article
- IL-33 regulates Müller cell-mediated retinal inflammation and neurodegeneration in diabetic retinopathy.Disease models & mechanisms · 2023Article
- Forward genetic screening using fundus spot scale identifies an essential role for Lipe in murine retinal homeostasis.Communications biology · 2023Article
- Etiological Roles of p75Cells · 2023Article
- The OSE complotype and its clinical potential.Frontiers in immunology · 2022Review
- Interlink between Inflammation and Oxidative Stress in Age-Related Macular Degeneration: Role of Complement Factor H.Biomedicines · 2021Review
- The complement system in age-related macular degeneration.Cellular and molecular life sciences : CMLS · 2021Review
- Nucleoside reverse transcriptase inhibitors and Kamuvudines inhibit amyloid-β induced retinal pigmented epithelium degeneration.Signal transduction and targeted therapy · 2021Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
purposeVariants of complement factor H (Cfh) affecting short consensus repeats (SCRs) 6 to 8 increase the risk of age-related macular degeneration. Our aim was to explore the effect of expressing a Cfh variant on the in vivo susceptibility of the retina and RPE to oxidative stress and inflammation, using chimeric Cfh transgenic mice (chCfhTg).
methodsThe chCfhTg and age-matched C57BL/6J (B6) mice were subjected to oxidative stress by either normal aging, or by exposure to a combination of oral hydroquinone (0.8% HQ) and increased light. Eyes were collected for immunohistochemistry of RPE-choroid flat mounts and of retinal sections, ELISA, electron microscopy, and RPE/microglia gene expression analysis.
resultsAging mice to 2 years led to an increased accumulation of basal laminar deposits, subretinal microglia/macrophages (MG/MΦ) staining for CD16 and for malondialdehyde (MDA), and MDA-modified proteins in the retina in chCfhTg compared to B6 mice. The chCfhTg mice maintained on HQ diet and increased light showed greater deposition of basal laminar deposits, more accumulation of fundus spots suggestive of MG/MΦ, and increased deposition of C3d in the sub-RPE space, compared to controls. In addition, chCfhTg mice demonstrated upregulation of NLRP3, IP-10, CD68, and TREM-2 in the RNA isolates from RPE/MG/MΦ.
conclusionsExpression of a Cfh transgene introducing a variant in SCRs 6 to 8 was sufficient to lead to increased retinal/RPE susceptibility to oxidative stress, a proinflammatory MG/MΦ phenotype, and a proinflammatory RPE/MG/MΦ gene expression profile in a transgenic mouse model. Our data suggest that altered interactions of Cfh with MDA-modified proteins may be relevant in explaining the effects of the Cfh variant.
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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 Socratic graph.