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Abnormal Reactivity of Müller Cells after Retinal Detachment in Mice Deficient in GFAP and Vimentin

¹From the Neuroscience Research Institute, ²Center for Bio-Image Informatics, and ⁶Department of Molecular, Cellular, and Developmental Biology, University of California, Santa Barbara, California; the ³Department of Ophthalmology, Asahikawa Medical College, Asahikawa, Japan; the ⁴Center for Brain Repair and Rehabilitation, Department of Clinical Neuroscience and Rehabilitation, Institute of Neuroscience and Physiology, Sahlgrenska, Academy at Göteborg University, Göteborg, Sweden; and the ⁵Schepens Eye Research Institute, Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts.

PURPOSE. To determine the roles of glial fibrillary acidic protein (GFAP) and vimentin in Müller cell reactivity.

METHODS. Retinal detachments were created in mice deficient for GFAP and vimentin (GFAP^–/–vim^–/–) and age-matched wild-type (wt) mice. The reactivity of the retina was studied by immunofluorescence and electron microscopy.

RESULTS. Müller cell morphology was different and glutamine synthetase immunoreactivity was reduced in the undisturbed GFAP^–/–vim^–/– retinas. After retinal detachment, Müller cells formed subretinal glial scars in the wt mice. In contrast, such scars were not observed in GFAP^–/–vim^–/– mice. Müller cells, which normally elongate and thicken in response to detachment, appeared compressed, thin, and "spikey" in the GFAP^–/–vim^–/– mice. The end foot region of Müller cells in the GFAP^–/–vim^–/– mice often sheared away from the rest of the retina during detachment, corroborating earlier results showing decreased resistance of this region in GFAP^–/–vim^–/– retinas to mechanical stress. In regions with end foot shearing, ganglion cells showed intense neurite sprouting, as revealed by anti–neurofilament labeling, a response rarely observed in wt mice.

CONCLUSIONS. Müller cells are subtly different in the GFAP^–/–vim^–/– mouse retina before detachment. The end foot region of these cells may be structurally reinforced by the presence of the intermediate filament cytoskeleton, and our data suggest a critical role for these proteins in Müller cell reaction to retinal detachment and participation in subretinal gliosis.