GONUTS has been updated to MW1.31 Most things seem to be working but be sure to report problems.

Have any questions? Please email us at ecoliwiki@gmail.com


Jump to: navigation, search


You don't have sufficient rights on this wiki to edit tables. Perhaps you need to log in. Changes you make in the Table editor will not be saved back to the wiki

See Help for Help on this wiki. See the documentation for how to use the table editor


Bora, NS, Kaliappan, S, Jha, P, Xu, Q, Sivasankar, B, Harris, CL, Morgan, BP and Bora, PS (2007) CD59, a complement regulatory protein, controls choroidal neovascularization in a mouse model of wet-type age-related macular degeneration. J. Immunol. 178:1783-90


We have shown that membrane attack complex (MAC) formation via the activation of the alternative pathway plays a central role in the laser-induced choroidal neovascularization (CNV). This study was undertaken to understand the role of a complement regulatory protein, CD59, which controls MAC assembly and function, in this model. CNV was induced by laser photocoagulation in C57BL/6 and Cd59a(-/-) mice using an argon laser. Animals from each group were sacrificed on day 1, 3, 5, and 7 postlaser. Retinal pigment epithelium-choroid-scleral tissue was examined to determine the incidence and size of CNV complex, and semiquantitative RT-PCR and Western blot analysis for CD59a was studied. Recombinant soluble mouse CD59a-IgG2a fusion (rsCD59a-Fc) protein was injected via i.p. or intravitreal routes 24 h before laser. Our results demonstrated that CD59a (both mRNA and protein) was down-regulated during laser-induced CNV. Cd59a(-/-) mice developed CNV complex early in the disease process. Increased MAC deposition was also observed in these Cd59a(-/-) mice. Administration of rsCD59a-Fc inhibited the development of CNV complex in the mouse model by blocking MAC formation and also inhibited expression of angiogenic growth factors. These data provide strong evidence that CD59a plays a crucial role in regulating complement activation and MAC formation essential for the release of growth factors that drive the development of laser-induced CNV in mice. Thus, our results suggest that the inhibition of complement by soluble CD59 may provide a novel therapeutic alternative to current treatment.




Animals; Antigens, CD59/analysis; Antigens, CD59/genetics; Antigens, CD59/physiology; Antigens, CD59/therapeutic use; Choroidal Neovascularization/drug therapy; Choroidal Neovascularization/etiology; Complement Activation; Complement Membrane Attack Complex; Disease Models, Animal; Down-Regulation; Immunoglobulin G/genetics; Intercellular Signaling Peptides and Proteins; Lasers/adverse effects; Macular Degeneration/etiology; Macular Degeneration/pathology; Macular Degeneration/therapy; Mice; Mice, Knockout; Recombinant Fusion Proteins/administration & dosage; Recombinant Fusion Proteins/pharmacology