The influence of age on apoptotic and other mechanisms of cell death after cerebral hypoxia-ischemia

被引:337
作者
Zhu, C
Wang, X
Xu, F
Bahr, BA
Shibata, M
Uchiyama, Y
Hagberg, H
Blomgren, K
机构
[1] Univ Gothenburg, Perinatal Ctr, Dept Physiol, SE-40530 Gothenburg, Sweden
[2] Zhengzhou Univ, Affiliated Hosp Ctr, Dept Pediat, Zhengzhou, Peoples R China
[3] Univ Connecticut, Dept Pharmaceut Sci, Storrs, CT USA
[4] Univ Connecticut, Program Neurosci, Storrs, CT USA
[5] Osaka Univ, Grad Sch Med, Dept Cell Biol & Neurosci, Osaka, Japan
[6] Sahlgrens Univ Hosp, Dept Obstet & Gynecol, S-41345 Gothenburg, Sweden
[7] Queen Silvia Childrens Hosp, Dept Pediat, Gothenburg, Sweden
基金
中国国家自然科学基金;
关键词
apoptosis-inducing factor (AIF); autophagy; caspase; calpain; cytochrome c; nitrotyrosine; hypoxia-ischemia; brain development;
D O I
10.1038/sj.cdd.4401545
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
Unilateral hypoxia-ischemia (HI) was induced in C57/BL6 male mice on postnatal day (P) 5, 9, 21 and 60, corresponding developmentally to premature, term, juvenile and adult human brains, respectively. HI duration was adjusted to obtain a similar extent of brain injury at all ages. Apoptotic mechanisms (nuclear translocation of apoptosis-inducing factor, cytochrome c release and caspase-3 activation) were several-fold more pronounced in immature than in juvenile and adult brains. Necrosis-related calpain activation was similar at all ages. The CA1 subfield shifted from apoptosis-related neuronal death at P5 and P9 to necrosis-related calpain activation at P21 and P60. Oxidative stress (nitrotyrosine formation) was also similar at all ages. Autophagy, as judged by the autophagosome-related marker LC-3 II, was more pronounced in adult brains. To our knowledge, this is the first report demonstrating developmental regulation of AIF-mediated cell death as well as involvement of autophagy in a model of brain injury.
引用
收藏
页码:162 / 176
页数:15
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