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Y Yamazaki, H Yamada, E Yamada, A Tsumura, M Matsumura; Apoptosis Cascade in Hyperoxia-induced Photoreceptor Cell Death . Invest. Ophthalmol. Vis. Sci. 2002;43(13):4521.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose: Hyperoxia causes vascular endothelial cell and photoreceptor cell dropout in the mouse retina. We previously demonstrated that hyperoxic photoreceptor cell death starts around day 5 of oxygen exposure and peaks on day 7. Our purpose in this study is to investigate the mechanisms by which these cells die from hyperoxic stress in vivo. Methods: C57bl/6j mice were exposed to a 75% concentration of oxygen for 1, 2 or 3 weeks. After the exposure, the mice were sacrificed and enucleated. Retinas were isolated from the eyeballs, homogenized, and processed for protein isolation. To quantify the protein levels of each apoptosis-associated protein, we performed Western blotting using antibodies against FAS, FAS-L, Bax, Bcl-2, Caspase 3, Caspase 8, and Caspase 9. To further investigate the role of Fas and Fas-L proteins in this apoptosis pathway, we exposed FAS knockout mice and FAS-L knockout mice to hyperoxic conditions and quantified the TUNEL index from their retinal sections. Results:Western blotting revealed upregulation of Caspase 3 and Bax in the retinas after one week of exposure to hyperoxia. The FAS and FAS-L knockout mice exposed to hyperoxia showed no difference in the TUNEL index compared to a wild-type mouse control. Conclusion:The mechanisms by which apoptosis occurs in photoreceptor cells following exposure to hyperoxia is still unclear, but upregulation of Bax may play a key role in the apoptosis cascade. FAS and FAS-L are unlikely to be involved in photoreceptor apoptosis caused by hyperoxia.
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