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Kirsten A. Wunderlich, Eberhart Zrenner, Maria-Thereza Perez; The Impact Of Glial Cell Reactivity On The Progression Of Photoreceptor Cell Loss In A Model Of Retinitis Pigmentosa. Invest. Ophthalmol. Vis. Sci. 2011;52(14):1875.
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Glial cell activation is characterized by proliferation and up-regulation of several molecules, including the intermediate filaments (IFs), glial fibrillary acidic protein (GFAP) and vimentin (Vim). Commonly used as markers for reactive gliosis, their function in the process has yet to be unraveled. In this study, we have investigated whether the inability to produce these IFs might affect photoreceptor cell degeneration.
Two groups of animals were studied: mice with retinal degeneration (PDE6β mutation, rd1) expressing GFAP and Vim (rd1, GFAP+/+Vim+/+) and mice with retinal degeneration and lacking the IFs (rd1, GFAP-/-Vim-/-). Retinas from postnatal day 7 (P7) to P60 mice were processed for histopathological examination, immunocytochemistry and Western Blot analysis of photoreceptor and glial cell markers.
No differences were noted in the distribution of rod or cone cell markers or in the number of dying cells in the outer nuclear layer at a given age in the two groups of rd1 mice. The expression of various Müller cell markers, including the cyclin kinase inhibitor p27Kip1, was also similar in both groups.
Previous studies have shown improved neuronal survival in association with the inability to produce and up-regulate GFAP and Vim. In the retina, a delay in photoreceptor cell loss, along with reduced glial reactivity, has been noted following retinal detachment. The present study shows, on the other hand, that the absence of the IFs did not result in photoreceptor rescue in the rd1 mouse. Further, a down-regulation of p27Kip1 has been shown to precede proliferation of Müller cells and up-regulation of GFAP in models of retinal damage. Our study shows that despite the inability to up-regulate GFAP in response to photoreceptor cell loss, the expression of p27Kip1 is unaltered, at least in the model of degeneration investigated.
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