Release of mitochondrial cytochrome c and DNA fragmentation after cold injury-induced brain trauma in mice: possible role in neuronal apoptosis

被引：41

作者：

Morita-Fujimura, Y

Fujimura, M

Kawase, M

Chen, SF

Chan, PH ^{[1
]}

机构：

[1] Stanford Univ, Sch Med, Dept Neurosurg, Palo Alto, CA 94304 USA

[2] Stanford Univ, Sch Med, Dept Neurol & Neurol Sci, Palo Alto, CA 94304 USA

[3] Stanford Univ, Sch Med, Program Neurosci, Palo Alto, CA 94304 USA

[4] Stanford Univ, Sch Med, Dept Neurol Surg, Palo Alto, CA 94304 USA

[5] Univ Calif San Francisco, Dept Neurol, San Francisco, CA 94143 USA

来源：

NEUROSCIENCE LETTERS | 1999年 / 267卷 / 03期

关键词：

cold injury; cytochrome c; traumatic brain injury; apoptosis; mitochondrial injury; caspase;

D O I：

10.1016/S0304-3940(99)00327-4

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Recent studies have shown that release of mitochondrial cytochrome c is a critical step in the apoptosis process. In this study, we examined the subcellular distribution of the cytochrome c protein after cold injury (Cl), in which apoptosis is assumed to participate. Western blotting and immunohistochemistry showed cytosolic cytochrome c as early as 1 h after Cl, and correspondingly, there was a reduction in mitochondrial cytochrome c after injury. Neuronal distribution of cytosolic cytochrome c was shown by double staining with a neuronal nuclear marker by immunohistochemistry. A significant amount of DNA laddering was detected 4 h after Cl, and increased in a time-dependent manner. These data suggest that early cytochrome c release from mitochondria may contribute to apoptosis induction after traumatic brain injury. (C) 1999 Elsevier Science Ireland Ltd. All rights reserved.

引用

页码：201 / 205

页数：5

共 21 条

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