title: Red light of the visual spectrum attenuates cell death in culture and retinal ganglion cell death in situ.
abstract: OBJECTIVE
  To ascertain whether red light, known to enhance mitochondrial function, can blunt chemical insults to cell cultures and ischaemic insults to the rat retina.
  
  
  METHODS
  Raised intraocular pressure (IOP, 140 mmHg, 60 min) or ischaemia was delivered in complete darkness or in the presence of low intensity red light (16.5 watts/m(2) , 3000 lux, 625-635 nm) to one eye of each rat. Animals were killed at specific times after ischemia and retinas analysis for ganglion cell numbers, the localization of specific antigens or for changes in defined RNAs. RGC-5 cell cultures were also exposed to various chemical insults in the presence or absence of red light. Significant differences were determined by t-test and anova.
  
  
  RESULTS
  Elevation of IOP causes changes in the localization of glial fibrillary acid protein (GFAP), calretinin, calbindin, choline acetyltransferase, ganglion cell numbers and an elevation (GFAP, vimentin, HO-1 and mTORC1) or reduction (Thy-1 and Brn3a) of mRNAs in the rat retina. These negative effects to the rat retina caused by ischaemia are reduced by red light. Moreover, chemical insults to cell cultures are blunted by red light.
  
  
  CONCLUSIONS
  Low, non-toxic levels of red light focussed on the retina for a short period of time are sufficient to attenuate an insult of raised IOP to the rat retina. Since mitochondrial dysfunctions are thought to play a major role in ganglion cell death in glaucoma, we propose the potential use of red light therapy for the treatment of the disease.
authors.affiliation: Eye Research Foundation, Oviedo, Spain.
authors.forename: Susana
authors.initials: S
authors.lastname: Del Olmo-Aguado
authors.affiliation: Eye Research Foundation, Oviedo, Spain.
authors.forename: Claudia
authors.initials: C
authors.lastname: Núñez-Álvarez
authors.affiliation: Eye Research Foundation, Oviedo, Spain.
authors.forename: Neville N
authors.initials: NN
authors.lastname: Osborne
mesh_terms: D000818:Animals; D017209:Apoptosis; D015415:Biomarkers / Q000378:metabolism; D015153:Blotting, Western; D002461:Cell Line, Transformed; D002470:Cell Survival; D002478:Cells, Cultured; D004791:Enzyme Inhibitors / Q000633:toxicity; D005047:Etoposide / Q000633:toxicity; D019084:Fluorescent Antibody Technique, Indirect; D006419:Heme Oxygenase (Decyclizing) / Q000235:genetics; D008027:Light; D008297:Male; D008856:Microscopy, Fluorescence; D012333:RNA, Messenger / Q000235:genetics; D051381:Rats; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000378:metabolism / Q000517:prevention & control*; D012160:Retina / Q000187:drug effects / Q000528:radiation effects*; D058499:Retinal Dystrophies / Q000378:metabolism / Q000517:prevention & control*; D012165:Retinal Ganglion Cells / Q000378:metabolism / Q000473:pathology*; D019810:Sodium Azide / Q000633:toxicity; D059005:Topoisomerase II Inhibitors / Q000633:toxicity
chemical_list: D015415:Biomarkers; D004791:Enzyme Inhibitors; D012333:RNA, Messenger; D059005:Topoisomerase II Inhibitors; D005047:Etoposide; D019810:Sodium Azide; D006419:Heme Oxygenase (Decyclizing); C491523:Hmox1 protein, rat
keywords: cell cultures; ganglion cells; mitochondria; neuroprotection; red light; retinal ischaemia