title: Remote Ischemic Preconditioning Protects Retinal Photoreceptors: Evidence From a Rat Model of Light-Induced Photoreceptor Degeneration.
abstract: OBJECTIVE
  To test whether remote ischemic preconditioning (RIP) is protective to photoreceptors, in a light damage model, and to identify mechanisms involved.
  
  
  METHODS
  A pressure cuff was used to induce ischemia (2 × 5 minutes) in one hind limb of 4- to 6-month-old albino Sprague-Dawley rats raised in dim, cyclic light (12 hours 5 lux, 12 hours dark). Immediately following the ischemia, rats were exposed to bright continuous light (1000 lux) for 24 hours. After 7-day survival in dim, cyclic light conditions, retinal function was assessed using the flash electroretinogram (ERG) and retinal structure was examined for photoreceptor survival and death, as well as for stress. Messenger RNA and protein expression of growth factors and brain-derived neurotrophic factor (BDNF) receptors was also assessed at 7-day survival.
  
  
  RESULTS
  Bright light exposure reduced the amplitude of the a- and b-waves of the ERG, upregulated the expression of glial fibrillary acidic protein (GFAP) by Müller cells, increased the number of dying (TUNEL+) photoreceptors, and reduced the number of surviving photoreceptors. Remote ischemic preconditioning mitigated all of these bright light-induced effects. Remote ischemic preconditioning-induced protection was associated with increased retinal expression of BDNF and its low-affinity receptor NGFR.
  
  
  CONCLUSIONS
  The present study provides evidence, for the first time, that RIP protects photoreceptors against bright light-induced photoreceptor degeneration. This observation is consistent with previous reports of RIP-induced protection of the inner retina and of other vital organs. Brain-derived neurotrophic factor may play a role in mediating the RIP-induced neuroprotection through activation of NGFR.
authors.affiliation: Bosch Institute and Discipline of Physiology, University of Sydney, Australia.
authors.forename: Alice
authors.initials: A
authors.lastname: Brandli
authors.affiliation: Bosch Institute and Discipline of Physiology, University of Sydney, Australia.
authors.forename: Daniel M
authors.initials: DM
authors.lastname: Johnstone
authors.affiliation: Bosch Institute and Discipline of Physiology, University of Sydney, Australia.
authors.forename: Jonathan
authors.initials: J
authors.lastname: Stone
mesh_terms: D000818:Animals; D015153:Blotting, Western; D019208:Brain-Derived Neurotrophic Factor / Q000096:biosynthesis / Q000235:genetics*; D016923:Cell Death; D004596:Electroretinography; D004797:Enzyme-Linked Immunosorbent Assay; D020287:In Situ Nick-End Labeling; D019194:Ischemic Preconditioning / Q000379:methods*; D008027:Light / Q000009:adverse effects*; D020419:Photoreceptor Cells, Vertebrate / Q000378:metabolism* / Q000473:pathology; D012313:RNA / Q000235:genetics*; D011833:Radiation Injuries, Experimental; D051381:Rats; D017207:Rats, Sprague-Dawley; D060888:Real-Time Polymerase Chain Reaction; D012162:Retinal Degeneration / Q000235:genetics / Q000378:metabolism / Q000517:prevention & control*; D020133:Reverse Transcriptase Polymerase Chain Reaction
chemical_list: D019208:Brain-Derived Neurotrophic Factor; D012313:RNA