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M. A. Tackenberg, J. S. Swift, B. A. Tucker, C. Jiang, M. Young; Müller Cell Activation and Proliferation Following Laser Injury. Invest. Ophthalmol. Vis. Sci. 2008;49(13):5189.
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It has previously been suggested that retinal injury, such as that induced by direct delivery of NMDA, can stimulate Müller glia to re-enter the cell cycle, proliferate and differentiate into a variety of retinal cell types, including bipolar cells and rod photoreceptors (Ooto et al., 2004, PNAS 101: 13654-13659). This suggests that Müller cells can potentially be induced to function as an endogenous source of progenitors aiding in adult retinal regeneration. Retinal laser photocoagulation, a commonly used clinical technique, may therefore become a method for injury induction and stimulation of such a response. The purpose of this study was to examine the effect of laser-induced damage to the outer photoreceptor layer of the mouse retina on Müller cell function and activity.
C57BL/6 mice were used as laser burn recipients and non-injured controls. Both groups of mice were euthanased and eyes enucleated at zero through seven days post laser burn and processed using immunohistochemistry and Western Blotting. Antibodies directed against Müller cells markers (GS, vimentin, GFAP, and CRALBP) the progenitor cell markers nestin and PAX-6, and the cell cycle cell markers Cyclin D1 and D3 were used.
Following laser injury, Müller cells positive for the markers GS, Vimentin and CRALBP, begin to upregulate their expression of the glial cell marker GFAP, the cell cycle marker Cyclin D1 and the progenitor cell marker nestin.
Our findings indicate that acute laser injury of the retinal outer nuclear layer stimulates reactivity, enhanced proliferation and potentially induction of "stemness" in host Müller glial cells.
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