title: Abnormal reactivity of muller cells after retinal detachment in mice deficient in GFAP and vimentin.
abstract: OBJECTIVE
  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.
authors.affiliation: Neuroscience Research Institute, University of California, Santa Barbara, California 93106, USA. mark.vera@sbcglobal.net
authors.forename: Mark R
authors.initials: MR
authors.lastname: Verardo
authors.forename: Geoffrey P
authors.initials: GP
authors.lastname: Lewis
authors.forename: Masumi
authors.initials: M
authors.lastname: Takeda
authors.forename: Kenneth A
authors.initials: KA
authors.lastname: Linberg
authors.forename: Jiyun
authors.initials: J
authors.lastname: Byun
authors.forename: Gabriel
authors.initials: G
authors.lastname: Luna
authors.forename: Ulrika
authors.initials: U
authors.lastname: Wilhelmsson
authors.forename: Milos
authors.initials: M
authors.lastname: Pekny
authors.forename: Dong-Feng
authors.initials: DF
authors.lastname: Chen
authors.forename: Steven K
authors.initials: SK
authors.lastname: Fisher
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D019084:Fluorescent Antibody Technique, Indirect; D005904:Glial Fibrillary Acidic Protein; D005974:Glutamate-Ammonia Ligase / Q000378:metabolism; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D018613:Microscopy, Confocal; D046529:Microscopy, Electron, Transmission; D009419:Nerve Tissue Proteins / Q000502:physiology*; D009457:Neuroglia / Q000378:metabolism* / Q000473:pathology; D020419:Photoreceptor Cells, Vertebrate / Q000378:metabolism / Q000473:pathology; D012160:Retina / Q000378:metabolism* / Q000473:pathology; D051245:Retinal Bipolar Cells / Q000378:metabolism / Q000473:pathology; D012163:Retinal Detachment / Q000378:metabolism* / Q000473:pathology; D012165:Retinal Ganglion Cells / Q000378:metabolism / Q000473:pathology; D051248:Retinal Horizontal Cells / Q000378:metabolism / Q000473:pathology; D017299:Rod Opsins / Q000378:metabolism; D009418:S100 Proteins / Q000378:metabolism; D015854:Up-Regulation; D014746:Vimentin / Q000502:physiology*
chemical_list: D005904:Glial Fibrillary Acidic Protein; D009419:Nerve Tissue Proteins; D017299:Rod Opsins; D009418:S100 Proteins; D014746:Vimentin; C528900:glial fibrillary astrocytic protein, mouse; D005974:Glutamate-Ammonia Ligase