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

被引:37
作者
Hahn, P
Lindsten, T
Lyubarsky, A
Ying, GS
Pugh, EN
Thompson, CB
Dunaief, JL
机构
[1] Univ Penn, FM Kirby Ctr Mol Ophthalmol, Philadelphia, PA 19104 USA
[2] Univ Penn, Scheie Eye Inst, Philadelphia, PA 19104 USA
[3] Univ Penn, Dept Med, Abramson Family Canc Res Inst, Philadelphia, PA 19104 USA
[4] Univ Penn, Dept Pathol, Abramson Family Canc Res Inst, Philadelphia, PA 19104 USA
[5] Univ Penn, Dept Lab Med, Abramson Family Canc Res Inst, Philadelphia, PA 19104 USA
关键词
Bax; Bak; apoptosis; light damage; photoreceptors; protection;
D O I
10.1038/sj.cdd.4401486
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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.
引用
收藏
页码:1192 / 1197
页数:6
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