title: Loss of BCL-XL in rod photoreceptors: Increased susceptibility to bright light stress.
abstract: OBJECTIVE
  BCL-X(L), an anti-apoptotic member of the BCL-2 family proteins and a cell death/survival checkpoint regulator, was shown to be upregulated in bright light-stressed mouse photoreceptors during an investigation of bright light-induced protein expression. To investigate the significance of BCL-X(L) upregulation in the bright light damage model, the Bcl-x gene was disrupted specifically in mouse rod photoreceptors, and the effect of Bcl-x disruption was characterized on retinal apoptosis, function, and morphology.
  
  
  METHODS
  Rod-specific Bcl-x knockout mice, generated by mating mouse opsin promoter-controlled Cre mice with floxed Bcl-x mice, were subjected to bright light stress. Retinal apoptosis in the bright light-stressed conditional Bcl-x knockout mice was characterized with TUNEL, DNA fragmentation, and nuclear staining assays. Photoreceptor structural and functional integrity in the bright light-stressed conditional Bcl-x knockout mice was determined by measuring photoreceptor outer nuclear layer (ONL) thickness and electroretinography amplitudes.
  
  
  RESULTS
  Disruption of Bcl-x in rod photoreceptors caused increased photoreceptor apoptosis, decreased retinal function, and decreased ONL thickness in bright light-stressed mice.
  
  
  CONCLUSIONS
  The loss of BCL-X(L) increased rod photoreceptor susceptibility to bright light stress. Although the biochemical mechanism(s) of BCL-X(L) in photoreceptor death or survival has not been investigated extensively, results of the present study suggest that BCL-X(L), a cell survival/death checkpoint regulator, is involved in photoreceptor survival under bright light stress.
authors.affiliation: Department of Ophthalmology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, USA.
authors.forename: Lixin
authors.initials: L
authors.lastname: Zheng
authors.forename: Robert E
authors.initials: RE
authors.lastname: Anderson
authors.forename: Martin-Paul
authors.initials: MP
authors.lastname: Agbaga
authors.forename: Edmund B
authors.initials: EB
authors.lastname: Rucker
authors.forename: Yun-Zheng
authors.initials: YZ
authors.lastname: Le
mesh_terms: D000818:Animals; D017209:Apoptosis; D015153:Blotting, Western; D053938:DNA Fragmentation; D004596:Electroretinography; D005260:Female; D007124:Immunoenzyme Techniques; D020287:In Situ Nick-End Labeling; D008027:Light; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D018345:Mice, Knockout; D018384:Oxidative Stress; D011833:Radiation Injuries, Experimental / Q000209:etiology* / Q000378:metabolism / Q000473:pathology; D012162:Retinal Degeneration / Q000209:etiology* / Q000378:metabolism / Q000473:pathology; D017948:Retinal Rod Photoreceptor Cells / Q000473:pathology / Q000528:radiation effects*; D051020:bcl-X Protein / Q000502:physiology*
chemical_list: C494812:Bcl2l1 protein, mouse; D051020:bcl-X Protein