title: Proliferative reactive gliosis is compatible with glial metabolic support and neuronal function.
abstract: BACKGROUND
  The response of mammalian glial cells to chronic degeneration and trauma is hypothesized to be incompatible with support of neuronal function in the central nervous system (CNS) and retina. To test this hypothesis, we developed an inducible model of proliferative reactive gliosis in the absence of degenerative stimuli by genetically inactivating the cyclin-dependent kinase inhibitor p27Kip1 (p27 or Cdkn1b) in the adult mouse and determined the outcome on retinal structure and function.
  
  
  RESULTS
  p27-deficient Müller glia reentered the cell cycle, underwent aberrant migration, and enhanced their expression of intermediate filament proteins, all of which are characteristics of Müller glia in a reactive state. Surprisingly, neuroglial interactions, retinal electrophysiology, and visual acuity were normal.
  
  
  CONCLUSIONS
  The benign outcome of proliferative reactive Müller gliosis suggests that reactive glia display context-dependent, graded and dynamic phenotypes and that reactivity in itself is not necessarily detrimental to neuronal function.
authors: Department of Ophthalmology and Visual Sciences, John A. Moran Eye Center, University of Utah, 65 Mario Capecchi Dr., Salt Lake City, UT 84132, USA.
authors: Félix R
authors: FR
authors: Vázquez-Chona
authors: Alex
authors: A
authors: Swan
authors: W Drew
authors: WD
authors: Ferrell
authors: Li
authors: L
authors: Jiang
authors: Wolfgang
authors: W
authors: Baehr
authors: Wei-Ming
authors: WM
authors: Chien
authors: Matthew
authors: M
authors: Fero
authors: Robert E
authors: RE
authors: Marc
authors: Edward M
authors: EM
authors: Levine
mesh_terms: D000818:Animals; D002454:Cell Differentiation / Q000502:physiology; D049109:Cell Proliferation; D004734:Energy Metabolism / Q000502:physiology; D005911:Gliosis / Q000378:metabolism* / Q000473:pathology; D051379:Mice; D018345:Mice, Knockout; D009410:Nerve Degeneration / Q000378:metabolism / Q000473:pathology*; D009457:Neuroglia / Q000378:metabolism* / Q000473:pathology; D009474:Neurons / Q000378:metabolism / Q000473:pathology / Q000502:physiology*; D012160:Retina / Q000378:metabolism / Q000473:pathology