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Lixin Zheng, Robert E. Anderson, Martin-Paul Agbaga, Edmund B. Rucker, Yun-Zheng Le; Loss of BCL-XL in Rod Photoreceptors: Increased Susceptibility to Bright Light Stress. Invest. Ophthalmol. Vis. Sci. 2006;47(12):5583-5589. https://doi.org/10.1167/iovs.06-0163.
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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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