ArticleGraefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie2013
ARMS2 interference leads to decrease of proinflammatory mediators.
Article in Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 16 citations in OpenAlex.
- Age-Related Maculopathy Susceptibility 2 and Complement Factor H Polymorphism and Intraocular Complement Activation in Neovascular Age-Related Macular Degeneration.Ophthalmology science · 2022Article
- Retinal Vessel Functionality Is Linked With ARMS2 A69S and CFH Y402H Polymorphisms and Choroidal Status in AMD Patients.Investigative ophthalmology & visual science · 2021Article
- Placenta Transcriptome Profiling in Intrauterine Growth Restriction (IUGR).International journal of molecular sciences · 2019Article
- Uncovering genetic and non-genetic biomarkers specific for exudative age-related macular degeneration: significant association of twelve variants.Oncotarget · 2018Article
- Notch signaling modulates proliferative vitreoretinopathy via regulating retinal pigment epithelial-to-mesenchymal transition.Histochemistry and cell biology · 2017Article
- Complement activation and choriocapillaris loss in early AMD: implications for pathophysiology and therapy.Progress in retinal and eye research · 2015Review
- Hyperthermia-induced upregulation of vascular endothelial growth factor in retinal pigment epithelial cells is regulated by mitogen-activated protein kinases.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2014Article
- Age-related macular degeneration: insights into inflammatory genes.Journal of ophthalmology · 2014Review
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAge-related macular degeneration (AMD) is a major cause of irreversible blindness among elderly people in developed countries. Many studies suggested that age-related maculopathy susceptibility 2 (ARMS2) is the second major susceptibility gene for AMD. Increasing evidence was found recently that inflammatory processes and oxidative stress may contribute to the pathogenesis of AMD. Meanwhile, the mechanisms underlying the contributions of ARMS2 to the pathogenesis of AMD remain unclear. The purpose of the current study was to elucidate the relationship between the ARMS2 gene and proinflammatory mediators, for further assessment of the associated biologic effects.
methodssiRNA was used to knock down ARMS2 mRNA, and Western blotting and reverse real-time PCR were used to detect the effect of siRNA on the expression of ARMS2 in ARPE-19 cells. The expressions of C3, C5, IL-6, IL-8, and TNF-α after si-RNA knockdown were evaluated by SYBR Green I real-time PCR and ELISA.
resultsTranscription accumulative indexes (TAI = 2(-delta delta CT)) of ARMS2 by real-time PCR revealed that the transfection rate in the positive control group was 72.0 ± 2.07 % (P < 0.01). The ratio of absorbance values (by Western blotting) of AMRS2 to β-actin was 0.85 ± 0.122, 0.87 ± 0.143, and 0.61 ± 0.240 in the blank control group, scrambled ARMS2-siRNA group, and ARMS2-siRNA group respectively (F = 42.5, P < 0.01). The secreted protein levels of C3, C5, IL-6, IL-8, and TNF-α were found by ELISA to be reduced by 34.24 ± 1.81 %, 37.15 ± 2.02 %, 35.11 ± 1.75 %, 30.11 ± 2.19 %, and 34.33 ± 2.18 % respectively, in the siRNA-ARMS2 group (P < 0.05). Compared with the blank control group, reduced TAI of C3, C5, IL-6, IL-8, and TNF-α were detected by real-time PCR in the ARMS2-siRNA group.
conclusionThis study produced evidence supporting the notion that the ARMS2 risk allele for AMD is linked directly or indirectly to proinflammatory mediators. More importantly, our data indicate that the change in ARMS2 may affect C3, C5, IL-6, IL-8, and TNF-α levels, and this may be one of the mechanisms of AMD development.
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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 OpenQuestion graph.