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M.H. Kuehn, C.Y. Kim, J. Ostojic, M. Bellin, D.S. Sakaguchi, S.D. Grozdanic, Y.H. Kwon; Complement Activation in Human and Experimental Glaucoma . Invest. Ophthalmol. Vis. Sci. 2006;47(13):417.
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Inappropriate activity of the complement cascade has been implicated in several neurodegenerative conditions. This study sought to determine if components of the complement cascade are synthesized in the retina during the progression of glaucoma and if complement accumulates in association with retinal ganglion cells.
Gene expression levels of complement components 1qb (C1qb) and 3 (C3) were determined in the retina by quantitative polymerase chain reaction (PCR) in human glaucomatous and healthy retinal tissue as well as in a rat model of glaucoma induced by laser cauterization of the trabecular meshwork and episcleral veins. Immunohistochemical methods were employed to determine the sites of complement deposition in the retina and optic nerve head.
Our data demonstrate that mRNA levels for C1q and C3 are significantly elevated in the glaucomatous retina when compared to healthy controls. Both C1q and C3 accumulate specifically in the retinal ganglion cell layer and the nerve fiber layer of glaucomatous eyes, but are typically absent in healthy control eyes. In addition, we demonstrate that the terminal complement complex, or membrane attack complex, is formed both in the human glaucomatous retina and in the rat model of glaucoma.
The expression of complement components and the formation of the membrane attack complex in the ganglion cell layer appear to be a part of the pathobiology of human glaucoma. Complement activation, particularly formation of membrane attack complexes, may have the potential to exacerbate ganglion cell death through bystander lysis or glial cell activation and could represent a contributing mechanism of damage in glaucoma.
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