Journal
INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE
Volume 47, Issue 12, Pages 5583-5589Publisher
ASSOC RESEARCH VISION OPHTHALMOLOGY INC
DOI: 10.1167/iovs.06-0163
Keywords
-
Categories
Funding
- NCRR NIH HHS [P20 RR017703, RR17703] Funding Source: Medline
- NEI NIH HHS [EY04149, EY12190, EY00871, P30 EY012190] Funding Source: Medline
Ask authors/readers for more resources
PURPOSE. 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
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available