Deficiency of Bax and Bak protects photoreceptors from light damage in vivo
Deficiency of Bax and Bak protects photoreceptors from light damage in vivo
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DOI：
10.1038/sj.cdd.4401486
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发表时间：
2004-11-01
影响因子：
12.4
通讯作者：
Dunaief, JL
中科院分区：
文献类型：
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作者：
Hahn, P;Lindsten, T;Dunaief, JL
bax（-/-）巴克（-/-）的光感受器，但bax（-/-）小鼠和巴克（-/-）小鼠均未受到发育性凋亡的保护，表明bax（-/-）巴克（-/-）光感受器也可能受到病理性凋亡的保护。为了测试这种可能性，我们将bax（-/-）巴克（-/-）和bax（-/-）小鼠暴露于强光下，这通常会诱导感光细胞死亡。与bax（-/-）小鼠相比，bax（-/-）巴克（-/-）小鼠中的光感受器免于死亡，如通过光损伤后24小时的TUNEL阳性光感受器核的数量减少和光损伤后7天的光感受器几乎完全保存所指示的。这些结果提供了第一个体内证据，即Bax和巴克的联合缺乏可以比Bax缺乏更有效地从病理刺激中拯救细胞，并表明Bax和巴克的联合缺乏也可以保护细胞免受其他损伤。
Photoreceptors of bax(-/-)bak(-/-) but neither bax(-/-) mice nor bak(-/-) mice are protected from developmental apoptosis, suggesting that bax(-/-)bak(-/-) photoreceptors may also be protected from pathologic apoptosis. To test this possibility, we exposed bax(-/-)bak(-/-) and bax(-/-) mice to bright light, which normally induces photoreceptor death. Photoreceptors in bax(-/-)bak(-/-) mice were protected from death compared to bax(-/-) mice as indicated by a reduction in the number of TUNEL-positive photoreceptor nuclei 24 h following light damage and almost complete preservation of photoreceptors 7 days following light damage. These results provide the first in vivo evidence that combined deficiency of Bax and Bak can rescue cells from a pathologic stimulus more effectively than Bax deficiency and suggest that combined deficiency of Bax and Bak may also protect cells from other insults.