NDLI: Aurintricarboxylic acid inhibits complement activation, membrane attack complex, and choroidal neovascularization in a model of macular degeneration.

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Aurintricarboxylic acid inhibits complement activation, membrane attack complex, and choroidal neovascularization in a model of macular degeneration.

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Aurintricarboxylic acid inhibits complement activation, membrane attack complex, and choroidal neovascularization in a model of macular degeneration.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Cashman, Siobhan M. Lipo, Erion Kumar-Singh, Rajendra
Description	Author Affiliation: Lipo E ( Department of Ophthalmology, Tufts University School of Medicine, Boston, Massachusetts.)
Abstract	PURPOSE: Immunocytochemical and genetic data implicate a significant role for the activation of complement in the pathology of AMD. Individuals homozygous for a Y402H polymorphism in Factor H have elevated levels of membrane attack complex (MAC) in their choroidal blood vessels and RPE relative to individuals homozygous for the wild-type allele. An R95X polymorphism in C9, a protein necessary for the final assembly of MAC, is partially protective against the formation of choroidal neovascularization (CNV) in AMD patients. Aurintricarboxylic Acid (ATA) is a small molecule inhibitor of MAC. Our hypothesis was that attenuation of the formation of MAC on ocular tissues by ATA may protect mice against laser-induced CNV. METHODS: The ability of ATA to inhibit human complement-mediated cell lysis, inhibit formation of human MAC, and inhibit formation of tubes by endothelial cells was examined in vitro. Subsequently, the Bruch's membrane of adult mice was damaged using an argon laser, followed by intravitreal injection of ATA. One week later, choroidal flat mounts from these mice were stained for the presence of MAC, endothelial cells, and macrophages. RESULTS: ATA protects cells from human complement-mediated lysis, attenuates assembly of the MAC, and inhibits tube formation by endothelial cells in vitro. ATA also attenuates CNV, MAC deposition, and macrophage infiltration in a murine model of exudative AMD. CONCLUSIONS: ATA warrants further study as a potential drug for the treatment of exudative and nonexudative AMD.
ISSN	01460404
e-ISSN	15525783
DOI	10.1167/iovs.13-12923
Journal	Investigative Opthalmology & Visual Science
Issue Number	10
Volume Number	54
Language	English
Publisher	Association for Research in Vision and Ophthalmology
Publisher Date	2013-10-29
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Aurintricarboxylic Acid Pharmacology Choroidal Neovascularization Prevention & Control Complement Membrane Attack Complex Antagonists & Inhibitors Macular Degeneration Complications Animals Apoptosis Drug Effects Cells, Cultured Disease Models, Animal Endothelial Cells Intravitreal Injections Mice Mice, Inbred C57bl Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't Research Support, U.s. Gov't, Non-p.h.s. Discipline Ophthalmology
Content Type	Text
Resource Type	Article
Subject	Ophthalmology Sensory Systems Cellular and Molecular Neuroscience

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