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Carsten Faber, Jennifer A. Williams, Stephen E. Moss, Mogens Holst Nissen, John Greenwood; Complement Factor H Lacks Regulatory Effects In Murine RPE. Invest. Ophthalmol. Vis. Sci. 2011;52(14):946.
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Age-related macular degeneration (AMD) is the commonest cause of blindness in the western world, affecting more than 10% of persons above 60 years of age. Although the pathogenesis is not known in detail, it involves formation of drusen and degeneration of the retinal pigment epithelium (RPE).Complement possibly plays a key role: drusen contains many complement proteins and a common variant of complement factor H (CFH) confers increased risk of developing AMD. To further characterize the role of complement in AMD, we analysed whether ocular complement activation depends on age and CFH.
Neuroretinas (NR) and RPE/choroid were isolated from young (~50 days) and old (~500 days) WT and Cfh-/- C57Bl/6 mice. RNA from two eyes/animal, four animals/group, was analysed with whole-transcript microarrays.
In RPE/choroid complement genes associated with both the classical and alternative pathway including C1, C2, C3, CFB were upregulated with age, whilst there was no differential regulation between genotypes. In NR, neither age nor genotype resulted in differential regulation.
In the RPE/choroid, complement activation increased with age independently of CFH. This implies that altered function of CFH is inconsequential to ocular complement activation, stressing the importance of systemic complement activation in AMD.
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