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Bax和Bak的缺失在体内可保护光感受器免受光损伤。

Deficiency of Bax and Bak protects photoreceptors from light damage in vivo.

作者信息

Hahn P, Lindsten T, Lyubarsky A, Ying G-S, Pugh E N, Thompson C B, Dunaief J L

机构信息

FM Kirby Center for Molecular Ophthalmology, University of Pennsylvania, Philadelphia, PA, USA.

出版信息

Cell Death Differ. 2004 Nov;11(11):1192-7. doi: 10.1038/sj.cdd.4401486.

Abstract

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.

摘要

bax基因敲除(-/-)/bak基因敲除(-/-)小鼠的光感受器,而非单独的bax基因敲除(-/-)小鼠或bak基因敲除(-/-)小鼠,可免受发育性细胞凋亡的影响,这表明bax基因敲除(-/-)/bak基因敲除(-/-)小鼠的光感受器也可能免受病理性细胞凋亡的影响。为了验证这种可能性,我们将bax基因敲除(-/-)/bak基因敲除(-/-)小鼠和bax基因敲除(-/-)小鼠暴露于强光下,强光通常会诱导光感受器死亡。与bax基因敲除(-/-)小鼠相比,bax基因敲除(-/-)/bak基因敲除(-/-)小鼠的光感受器可免受死亡影响,这表现为在光损伤后24小时,TUNEL阳性光感受器细胞核数量减少,以及在光损伤后7天光感受器几乎完全得以保存。这些结果提供了首个体内证据,表明Bax和Bak的联合缺陷比Bax缺陷更能有效地使细胞从病理性刺激中获救,并表明Bax和Bak的联合缺陷也可能保护细胞免受其他损伤。

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