ArticleJournal of neuroinflammation2017
Age-related macular degeneration associated polymorphism rs10490924 in ARMS2 results in deficiency of a complement activator.
Article in Journal of neuroinflammation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers, 3 of them syntheses that pooled it.
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Who cites it
60 citing papers in PubMed, 3 syntheses or guidelines pooled it, 100 citations in OpenAlex.
- A systematic review of gut microbiome and ocular inflammatory diseases: Are they associated?Indian journal of ophthalmology · 2021Pooled it
- Pooled it
- Periodontal Disease and Age-Related Macular Degeneration: A Meta-Analysis of 112,240 Participants.BioMed research international · 2020Pooled it
- Natural History of Drusenoid Pigment Epithelial Detachment Associated with Age-Related Macular Degeneration: Age-Related Eye Disease Study 2 Report No. 17.Ophthalmology · 2019Trial
- Progression of Geographic Atrophy in Age-related Macular Degeneration: AREDS2 Report Number 16.Ophthalmology · 2018Trial
- GWAS SVatalog: a visualization tool to aid fine-mapping of GWAS loci with structural variations.Heredity · 2026Article
- The Prevalence of Malnutrition and Early-Stage Age-Related Macular Degeneration: Using Three Nutritional Scoring Systems.Translational vision science & technology · 2025Article
- Genetic Associations of Rod- and Cone-Mediated Vision in Aging and Age-Related Macular Degeneration.Investigative ophthalmology & visual science · 2025Article
- A homogeneous immunoassay technology based on liposomes and the complement system enables one-step, no-wash, rapid diagnostics directly in serum.Analytical and bioanalytical chemistry · 2025Article
- HTRA1 and complement activation in neovascular age-related macular degeneration.Japanese journal of ophthalmology · 2025Article
- Genotypes of SNPs of key genes regulate susceptibility and drug sensitivity to neovascular AMD in the human population.BMJ open ophthalmology · 2025Article
- Adult Onset Foveomacular Vitelliform Dystrophy Shows Genetic Overlap With Age-Related Macular Degeneration.Investigative ophthalmology & visual science · 2024Article
- Complement proteins and complement regulatory proteins are associated with age-related macular degeneration stage and treatment response.Journal of neuroinflammation · 2024Article
- The hypothetical molecular mechanism of the ethnic variations in the manifestation of age-related macular degeneration; focuses on the functions of the most significant susceptibility genes.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2024Review
- Aging of the eye: Lessons from cataracts and age-related macular degeneration.Ageing research reviews · 2024Review
- Age- and sex- divergent translatomic responses of the mouse retinal pigmented epithelium.Neurobiology of aging · 2024Article
- Genetic Insights into Age-Related Macular Degeneration.Biomedicines · 2024Review
- Modeling complex age-related eye disease.Progress in retinal and eye research · 2024Review
- Recent Advances in Our Understanding of Age-Related Macular Degeneration: Mitochondrial Dysfunction, Redox Signaling, and the Complement System.Aging and disease · 2024Review
- The interactions betweenMolecular vision · 2024Article
Corrections and comments
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Authors and funding
20 authors at 7 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAge-related macular degeneration (AMD) is the leading cause of blindness in developed countries. The polymorphism rs10490924 in the ARMS2 gene is highly associated with AMD and linked to an indel mutation (del443ins54), the latter inducing mRNA instability. At present, the function of the ARMS2 protein, the exact cellular sources in the retina and the biological consequences of the rs10490924 polymorphism are unclear.
methodsRecombinant ARMS2 was expressed in Pichia pastoris, and protein functions were studied regarding cell surface binding and complement activation in human serum using fluoresence-activated cell sorting (FACS) as well as laser scanning microscopy (LSM). Biolayer interferometry defined protein interactions. Furthermore, endogenous ARMS2 gene expression was studied in human blood derived monocytes and in human induced pluripotent stem cell-derived microglia (iPSdM) by PCR and LSM. The ARMS2 protein was localized in human genotyped retinal sections and in purified monocytes derived from AMD patients without the ARMS2 risk variant by LSM. ARMS2 expression in monocytes under oxidative stress was determined by Western blot analysis.
resultsHere, we demonstrate for the first time that ARMS2 functions as surface complement regulator. Recombinant ARMS2 binds to human apoptotic and necrotic cells and initiates complement activation by recruiting the complement activator properdin. ARMS2-properdin complexes augment C3b surface opsonization for phagocytosis. We also demonstrate for the first time expression of ARMS2 in human monocytes especially under oxidative stress and in microglia cells of the human retina. The ARMS2 protein is absent in monocytes and also in microglia cells, derived from patients homozygous for the ARMS2 AMD risk variant (rs10490924).
conclusionsARMS2 is likely involved in complement-mediated clearance of cellular debris. As AMD patients present with accumulated proteins and lipids on Bruch's membrane, ARMS2 protein deficiency due to the genetic risk variant might be involved in drusen formation.
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