ArticleInvestigative ophthalmology & visual science2015
Local production of the alternative pathway component factor B is sufficient to promote laser-induced choroidal neovascularization.
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 32 papers.
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Who cites it
32 citing papers in PubMed.
- Complement Factor B Deficiency Is Dispensable for Female Fertility but Affects Microbiome Diversity and Complement Activity.International journal of molecular sciences · 2025Article
- Roles of MASP-1 and MASP-3 in the development of retinal degeneration in a murine model of dry age-related macular degeneration.Frontiers in immunology · 2025Article
- Recent Advances of Proteomics in Management of Acute Kidney Injury.Diagnostics (Basel, Switzerland) · 2023Review
- Bruch's Membrane: A Key Consideration with Complement-Based Therapies for Age-Related Macular Degeneration.Journal of clinical medicine · 2023Review
- Low-molecular weight inhibitors of the alternative complement pathway.Immunological reviews · 2023Review
- Dabigatran and Wet AMD, Results From Retinal Pigment Epithelial Cell Monolayers, the Mouse Model of Choroidal Neovascularization, and Patients From the Medicare Data Base.Frontiers in immunology · 2022Article
- Complement Factor B Mediates Ocular Angiogenesis through Regulating the VEGF Signaling Pathway.International journal of molecular sciences · 2021Article
- Targeting complement components C3 and C5 for the retina: Key concepts and lingering questions.Progress in retinal and eye research · 2021Review
- Complement System and Potential Therapeutics in Age-Related Macular Degeneration.International journal of molecular sciences · 2021Review
- Natural immunoglobulin M-based delivery of a complement alternative pathway inhibitor in mouse models of retinal degeneration.Experimental eye research · 2021Article
- Subretinal Rather Than Intravitreal Adeno-Associated Virus-Mediated Delivery of a Complement Alternative Pathway Inhibitor Is Effective in a Mouse Model of RPE Damage.Investigative ophthalmology & visual science · 2021Article
- Complement Inhibition Alleviates Cholestatic Liver Injury Through Mediating Macrophage Infiltration and Function in Mice.Frontiers in immunology · 2021Article
- Associations between the Complement System and Choroidal Neovascularization in Wet Age-Related Macular Degeneration.International journal of molecular sciences · 2020Review
- Functional Evaluation of AMD-Associated Risk Variants of Complement Factor B.Investigative ophthalmology & visual science · 2020Article
- Ablation of C3 modulates macrophage reactivity in the outer retina during photo-oxidative damage.Molecular vision · 2020Article
- Complement factor B knockdown by short hairpin RNA inhibits laser-induced choroidal neovascularization in rats.International journal of ophthalmology · 2020Article
- The use of Matrigel combined with encapsulated cell technology to deliver a complement inhibitor in a mouse model of choroidal neovascularization.Molecular vision · 2020Article
- Clinical promise of next-generation complement therapeutics.Nature reviews. Drug discovery · 2019Review
- Differential responses of Lasiopodomys mandarinus and Lasiopodomys brandtii to chronic hypoxia: a cross-species brain transcriptome analysis.BMC genomics · 2018Article
- Viral mimic polyinosine-polycytidylic acid potentiates liver injury in trichloroethylene-sensitized mice - Viral-chemical interaction as a novel mechanism.Ecotoxicology and environmental safety · 2018Article
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Authors and funding
8 authors.
Funding
Abstract
purposeComplement factor B (CFB) is a required component of the alternative pathway (AP) of complement, and CFB polymorphisms are associated with age-related macular degeneration (AMD) risk. Complement factor B is made in the liver, but expression has also been detected in retina and retinal pigment epithelium (RPE)-choroid. We investigated whether production of CFB by the RPE can promote AP activation in mouse choroidal neovascularization (CNV).
methodsTransgenic mice expressing CFB under the RPE65 promoter were generated and crossed onto factor B-deficient (CFB-KO) mice. Biological activity was determined in vitro using RPE monolayers and in vivo using laser-induced CNV. Contribution of systemic CFB was investigated using CFB-KO reconstituted with CFB-sufficient serum.
resultsTransgenic mice (CFB-tg) expressed CFB in RPE-choroid; no CFB was detected in serum. Cultured CFB-tg RPE monolayers secreted CFB apically and basally upon exposure to oxidative stress that was biologically active. Choroidal neovascularization sizes were comparable between wild-type and CFB-tg mice, but significantly increased when compared to lesions in CFB-KO mice. Injections of CFB-sufficient serum into CFB-KO mice resulted in partial reconstitution of systemic AP activity and significantly increased CNV size.
conclusionsMouse RPE cells express and secrete CFB sufficient to promote RPE damage and CNV. This further supports that local complement production may regulate disease processes; however, the reconstitution experiments suggest that additional components may be sequestered from the bloodstream. Understanding the process of ocular complement production and regulation will further our understanding of the AMD disease process and the requirements of a complement-based therapeutic.
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