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Oxidative Stress Renders Retinal Pigment Epithelial Cells Susceptible to Complement-mediated Injury*
Uncontrolled activation of the alternative pathway of complement is thought to be associated with age-related macular degeneration (AMD). The alternative pathway is continuously activated in theExpand
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A targeted inhibitor of the alternative complement pathway reduces angiogenesis in a mouse model of age-related macular degeneration.
PURPOSE Polymorphisms in factor H (fH), an inhibitor of the alternative pathway (AP) of complement activation, are associated with increased risk for age-related macular degeneration (AMD). TheExpand
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Eliminating complement factor D reduces photoreceptor susceptibility to light-induced damage.
PURPOSE Genetic risk factors such as variations in complement factors H (CFH) and B (CFB) have been implicated in the etiology of age-related macular degeneration. It has been hypothesized thatExpand
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Sublytic Membrane-Attack-Complex (MAC) Activation Alters Regulated Rather than Constitutive Vascular Endothelial Growth Factor (VEGF) Secretion in Retinal Pigment Epithelium Monolayers*
Uncontrolled activation of the alternative complement pathway and secretion of vascular endothelial growth factor (VEGF) are thought to be associated with age-related macular degeneration (AMD).Expand
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Oxidative Stress Sensitizes Retinal Pigmented Epithelial (RPE) Cells to Complement-mediated Injury in a Natural Antibody-, Lectin Pathway-, and Phospholipid Epitope-dependent Manner*
Background: Age-related macular degeneration (AMD) involves complement activation; however, initiating ligands and essential arms of the complement cascade are unknown. Results: PhospholipidExpand
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Apoptosis and Autophagy in Photoreceptors Exposed to Oxidative Stress
Studies on human and animal models of retinal dystrophy have suggested that apoptosis may be the common pathway of photoreceptor cell death. Autophagy, the major cellular degradation process inExpand
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The alternative pathway is required, but not alone sufficient, for retinal pathology in mouse laser-induced choroidal neovascularization.
Human genetic studies have demonstrated that polymorphisms in different complement proteins can increase the risk for developing AMD. There are three pathways of complement activation, classicalExpand
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A targeted inhibitor of the complement alternative pathway reduces RPE injury and angiogenesis in models of age-related macular degeneration.
Genetic variations in complement factor H (fH), an inhibitor of the complement alternative pathway (CAP), and oxidative stress are associated with age-related macular degeneration (AMD). Recently,Expand
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Cone outer segment morphology and cone function in the Rpe65-/- Nrl-/- mouse retina are amenable to retinoid replacement.
PURPOSE RPE65, a major retinal pigment epithelium protein, is essential in generating 11-cis retinal, the chromophore for all opsins. Without chromophore, cone opsins are mislocalized and conesExpand
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Paradoxical role of BDNF: BDNF+/- retinas are protected against light damage-mediated stress.
PURPOSE Photoreceptors can be prevented from undergoing apoptosis in response to constant light by the application of exogenous neuroprotective agents, including brain-derived neurotrophic factorExpand
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