May 2005
Volume 46, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2005
Glial Hypertrophy and Neuronal Remodeling in Mice Deficient in GFAP and Vimentin Following Experimental Retinal Detachment
Author Affiliations & Notes
  • M.R. Verardo
    Neuroscience Research Institute,
    University of California, Santa Barbara, CA
  • G.P. Lewis
    Neuroscience Research Institute,
    University of California, Santa Barbara, CA
  • M. Takeda
    Dept. of Ophthalmology, Schepens Eye Research Institute, Harvard Medical School, Boston, MA
  • B.M. Wardak
    Neuroscience Research Institute,
    University of California, Santa Barbara, CA
  • M.D. Rabena
    Neuroscience Research Institute,
    University of California, Santa Barbara, CA
  • D.F. Chen
    Dept. of Ophthalmology, Schepens Eye Research Institute, Harvard Medical School, Boston, MA
  • S.K. Fisher
    Neuroscience Research Institute and Dept. of MCD Biology,
    University of California, Santa Barbara, CA
  • Footnotes
    Commercial Relationships  M.R. Verardo, None; G.P. Lewis, None; M. Takeda, None; B.M. Wardak, None; M.D. Rabena, None; D.F. Chen, None; S.K. Fisher, None.
  • Footnotes
    Support  NEI EY0088 (SKF), NSF0331697 (SKF), NEI EY012983 (DFC), Dept. of Defense (DFC)
Investigative Ophthalmology & Visual Science May 2005, Vol.46, 2443. doi:
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      M.R. Verardo, G.P. Lewis, M. Takeda, B.M. Wardak, M.D. Rabena, D.F. Chen, S.K. Fisher; Glial Hypertrophy and Neuronal Remodeling in Mice Deficient in GFAP and Vimentin Following Experimental Retinal Detachment . Invest. Ophthalmol. Vis. Sci. 2005;46(13):2443.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Abstract: : Purpose: Retinal detachment induces Müller cell hypertrophy both within the retina and as cellular membranes in the subretinal space. Structural and immunolabeling data suggest a prominent role for the cytoskeleton in this process. Indeed, glial fibrillary acidic protein (GFAP), vimentin, and tubulin upregulation are all hallmarks of the hypertrophy. There also may be a relationship between Müller cell hypertrophy and neuronal remodeling after detachment. Here we sought to determine if Müller cell hypertrophy was functionally dependent upon the presence of the 2 intermediate filament proteins GFAP and vimentin. Methods: Experimental retinal detachments were created in wild–type C57BL/6J mice and mice deficient in GFAP and vimentin (GFAP–/–vim–/–). The retinas were harvested at 7 or 28 days post–detachment. Immunohistochemistry was performed using antibodies to GFAP, vimentin, S100, VAMP, rod opsin, cone opsins, protein kinase C, and neurofilament protein. Images were collected with an Olympus Fluoview confocal microscope. Results: Glial cell hypertrophy was observed in both wild–type and GFAP–/–vim–/– mice following detachment. Focal regions of Müller cell growth appeared sclerad to the outer limiting membrane in both groups after detachment. These processes were anti–GFAP, –S100, and –vimentin labeled in wild–type mice and only anti–S100 labeled in the GFAP–/–vim–/–. Anti–S100 labeling revealed abnormal Müller cell morphology in the attached GFAP–/–vim–/– retina, which was exaggerated after detachment. Extensive neuronal remodeling also occurred both in the GFAP–/–vim–/– and wild–type animals. These events included the sprouting of neurites from bipolar and horizontal cells into the outer nuclear layer. Conclusions: These studies demonstrate that the intermediate filament proteins GFAP and vimentin are not required for the hypertrophy of Müller cells nor does their absence prevent neuronal remodeling/sprouting in the GFAP–/–vim–/– retinas. The results suggest that other cytoskeleton protein(s) may play a critical role in initiating Müller cell hypertrophy.

Keywords: retinal detachment • Muller cells • transgenics/knock-outs 
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