title: Effects of ischemia-reperfusion on physiological properties of Müller glial cells in the porcine retina.
abstract: OBJECTIVE
  Transient retinal ischemia-reperfusion is associated with neuronal degeneration and activation of Müller glial cells. Reactive gliosis may impede the homeostatic functions of Müller cells. A viable animal model for human ischemic events should display similarities in eye size and retinal blood supply. Therefore, pigs were used in this investigation of physiological alterations in Müller cells after ischemia-reperfusion.
  
  
  METHODS
  Transient retinal ischemia was induced in young adult pigs by high intraocular pressure in one eye for 1 hour. After 3 days of reperfusion, the retinal tissue and isolated Müller cells were used for osmotic swelling recordings, whole-cell patch-clamp experiments, Ca(2+) microfluorimetry, and immunohistochemistry.
  
  
  RESULTS
  Müller cells in retinal slices from postischemic eyes but not control cells displayed a significant swelling of the somata when osmotic stress was applied by hypotonic extracellular solution. The amplitude of K(+) inward currents was significantly reduced (∼60% of the control value). This decrease was accompanied by a depolarization of the cell membrane. The number of Müller cell end feet displaying a Ca(2+) increase after application of adenosine 5'-triphosphate was increased in the ischemic retina. Moreover, reactive Müller cell gliosis was characterized by an (increased) expression of vimentin, glial fibrillary acidic protein, the phosphorylated mitogen-activated protein kinases extracellular signal-related kinase (ERK) 1 and 2, and the transcription factor c-fos.
  
  
  CONCLUSIONS
  The alterations of reactive Müller cells after transient ischemia of the pig eye were similar to those found in rat and rabbit models, demonstrating that the porcine retina is a suitable model for the investigation of ischemic injury.
authors.affiliation: Paul-Flechsig-Institut für Hirnforschung, Universität Leipzig, Jahnallee 59, 04109 Leipzig, Germany.
authors.forename: Antje
authors.initials: A
authors.lastname: Wurm
authors.forename: Ianors
authors.initials: I
authors.lastname: Iandiev
authors.forename: Susann
authors.initials: S
authors.lastname: Uhlmann
authors.forename: Peter
authors.initials: P
authors.lastname: Wiedemann
authors.forename: Andreas
authors.initials: A
authors.lastname: Reichenbach
authors.forename: Andreas
authors.initials: A
authors.lastname: Bringmann
authors.forename: Thomas
authors.initials: T
authors.lastname: Pannicke
mesh_terms: D000241:Adenosine / Q000378:metabolism; D000818:Animals; D051401:Aquaporin 4 / Q000378:metabolism; D002118:Calcium / Q000378:metabolism; D005260:Female; D005434:Flow Cytometry; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D005911:Gliosis / Q000188:drug therapy / Q000378:metabolism*; D005938:Glucocorticoids / Q000627:therapeutic use; D007150:Immunohistochemistry; D008297:Male; D019950:Mitogen-Activated Protein Kinase 1 / Q000378:metabolism; D048052:Mitogen-Activated Protein Kinase 3 / Q000378:metabolism; D009457:Neuroglia / Q000502:physiology*; D018408:Patch-Clamp Techniques; D024661:Potassium Channels, Inwardly Rectifying / Q000378:metabolism; D016760:Proto-Oncogene Proteins c-fos / Q000378:metabolism; D015427:Reperfusion Injury / Q000188:drug therapy / Q000378:metabolism*; D012164:Retinal Diseases / Q000188:drug therapy / Q000378:metabolism*; D012171:Retinal Vessels / Q000187:drug effects / Q000378:metabolism*; D013552:Swine; D014222:Triamcinolone Acetonide / Q000627:therapeutic use; D000098854:Kcnj10 Channel
chemical_list: D051401:Aquaporin 4; D005904:Glial Fibrillary Acidic Protein; D005938:Glucocorticoids; D000098854:Kcnj10 Channel; D024661:Potassium Channels, Inwardly Rectifying; D016760:Proto-Oncogene Proteins c-fos; D019950:Mitogen-Activated Protein Kinase 1; D048052:Mitogen-Activated Protein Kinase 3; D014222:Triamcinolone Acetonide; D000241:Adenosine; D002118:Calcium