title: The effect of ischemic preconditioning on light-induced photoreceptor injury.
abstract: OBJECTIVE
  To determine whether ischemic preconditioning (IPC) upregulates certain retinal survival factors and to assess the protective effect of retinal IPC against light-induced photoreceptor degeneration.
  
  
  METHODS
  Albino rats underwent IPC induced by raising the intraocular pressure in one eye to 120 mm Hg for 5 minutes. The fellow eye underwent sham treatment. Basic fibroblast growth factor (bFGF), ciliary neurotrophic factor (CNTF), brain-derived neurotrophic factor (BDNF), glial fibrillary acidic protein (GFAP), and Bcl-2 were measured after 6 and 48 hours, by the reverse transcription-polymerase chain reaction and immunoblot analysis. Other preconditioned rats received 48 hours of photic injury (2000 lux) 24 hours after IPC. The a- and b-wave amplitudes of the flash electroretinograms were measured 5 days later, followed by analysis of rhodopsin mRNA levels and histology. The influence of adenosine A1 receptor blockade was assessed.
  
  
  RESULTS
  bFGF, GFAP, and Bcl-2 were upregulated after IPC. BDNF was not upregulated. The marked reduction of the a- and b-wave amplitudes and the structural injury to the photoreceptors induced by the photic insult were significantly reduced by IPC. The protection afforded by IPC was not influenced by adenosine A1 antagonism.
  
  
  CONCLUSIONS
  IPC upregulates bFGF, GFAP, and Bcl-2 and protects photoreceptors against light-induced injury. These factors may be involved in the protective response.
authors.affiliation: Nuffield Laboratory of Ophthalmology, Oxford University, Oxford, United Kingdom.
authors.forename: Robert J
authors.initials: RJ
authors.lastname: Casson
authors.forename: John P M
authors.initials: JP
authors.lastname: Wood
authors.forename: Jose
authors.initials: J
authors.lastname: Melena
authors.forename: Glyn
authors.initials: G
authors.lastname: Chidlow
authors.forename: Neville N
authors.initials: NN
authors.lastname: Osborne
mesh_terms: D000818:Animals; D019208:Brain-Derived Neurotrophic Factor / Q000235:genetics / Q000378:metabolism; D020934:Ciliary Neurotrophic Factor / Q000235:genetics / Q000378:metabolism; D004596:Electroretinography; D005260:Female; D016222:Fibroblast Growth Factor 2 / Q000235:genetics / Q000378:metabolism; D005904:Glial Fibrillary Acidic Protein / Q000235:genetics / Q000378:metabolism; D019194:Ischemic Preconditioning; D008027:Light; D020419:Photoreceptor Cells, Vertebrate / Q000502:physiology / Q000528:radiation effects*; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000235:genetics / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D011833:Radiation Injuries, Experimental / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D051381:Rats; D017208:Rats, Wistar; D012162:Retinal Degeneration / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D012171:Retinal Vessels; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012243:Rhodopsin / Q000235:genetics / Q000378:metabolism; D015854:Up-Regulation
chemical_list: D019208:Brain-Derived Neurotrophic Factor; D020934:Ciliary Neurotrophic Factor; D005904:Glial Fibrillary Acidic Protein; D019253:Proto-Oncogene Proteins c-bcl-2; D012333:RNA, Messenger; D016222:Fibroblast Growth Factor 2; D012243:Rhodopsin