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Publication : Loss of BCL-XL in rod photoreceptors: Increased susceptibility to bright light stress.

First Author  Zheng L Year  2006
Journal  Invest Ophthalmol Vis Sci Volume  47
Issue  12 Pages  5583-9
PubMed ID  17122152 Mgi Jnum  J:123107
Mgi Id  MGI:3717064 Doi  10.1167/iovs.06-0163
Citation  Zheng L, et al. (2006) Loss of BCL-XL in rod photoreceptors: Increased susceptibility to bright light stress. Invest Ophthalmol Vis Sci 47(12):5583-9
abstractText  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.
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