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(Investigative Ophthalmology and Visual Science. 2006;47:5583-5589.)
© 2006 by The Association for Research in Vision and Ophthalmology, Inc.
doi:10.1167/iovs.06-0163
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Loss of BCL-XL in Rod Photoreceptors: Increased Susceptibility to Bright Light Stress

Lixin Zheng,1,2 Robert E. Anderson,1,2,3 Martin-Paul Agbaga,2,3 Edmund B. Rucker, III,4 and Yun-Zheng Le1,2,3

1From the Departments of Ophthalmology and 3Cell Biology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma; the 2Dean A. McGee Eye Institute, Oklahoma City, Oklahoma; and the 4Department of Animal Sciences, University of Missouri, Columbia, Missouri.

PURPOSE. BCL-XL, 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-XL 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-XL increased rod photoreceptor susceptibility to bright light stress. Although the biochemical mechanism(s) of BCL-XL in photoreceptor death or survival has not been investigated extensively, results of the present study suggest that BCL-XL, a cell survival/death checkpoint regulator, is involved in photoreceptor survival under bright light stress.




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