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S.K. Fisher, G.P. Lewis, K.C. Talaga, R.L. Avery; Differential Localization of Intermediate Filament Proteins in Subretinal and Epiretinal Müller Cells After Retinal Detachment and Reattachment . Invest. Ophthalmol. Vis. Sci. 2003;44(13):2958.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose: To compare the localization patterns of glial fibrillary acidic protein (GFAP) and vimentin, in Müller cells after experimental retinal detachment and reattachment. Methods: Detachments were created in the right eyes of domestic cats and tissue was harvested at 3 (n=2) or 7 (n=3) days after surgery. In 3 animals the retina was reattached on day 3 and tissue harvested 28 days later. Immunolabeled vibratome sections were viewed by laser scanning confocal microscopy. Results: In non-reactive Müller cells, intermediate filament proteins occur mostly in the end-foot and vimentin predominates over GFAP. Following detachment, the expression of both proteins increases throughout the Müller cell, but the balance shifts towards GFAP. Occasionally a Müller cell process in the outer retina appears intensely labeled for vimentin and it is these cells that grow through the outer limiting membrane to form subretinal glial scars. Vimentin always predominates at the edge of these subretinal membranes where growth may be occurring. Reattachment stops the subretinal growth of Müller cells but stimulates their growth into the vitreous cavity where they create the cellular membranes of proliferative vitreoretinopathy (PVR). The expression pattern for GFAP and vimentin in the epiretinal membranes is the opposite of that in the subretinal membranes; i.e., GFAP predominates, especially at the edge of the membrane. These patterns remains in long-term, complex subretinal and epiretinal membranes. The distribution of CD-44, a transmembrane glycoprotein, is also different on subretinal and epiretinal Müller cell processes. Although orientation relative to outgrowth from the retina is an issue, we have observed similar patterns of IF protein distribution in human epiretinal membranes. Conclusions: Müller cells regulate their expression of IF proteins (and CD-44) in specific, polarized patterns relating to their growth in the subretinal space or vitreous. This information may lead to mechanisms for controlling the growth of Müller cells in diseases such as subretinal fibrosis and PVR.
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