Release of mitochondrial cytochrome c and DNA fragmentation after cold injury-induced brain trauma in mice: possible role in neuronal apoptosis.
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 (CI), in which apoptosis is assumed to participate. Western blotting and immunohistochemistry showed cytosolic cytochrome c as early as 1 h after CI, 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 CI, 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.
Morita-Fujimura
Y
Y
Department of Neurosurgery, Stanford University School of Medicine, Palo Alto, CA 94304, USA.
Fujimura
M
M
Kawase
M
M
Chen
S F
SF
Chan
P H
PH
D000818:Animals; D017209:Apoptosis / Q000502:physiology; D001929:Brain Edema / Q000503:physiopathology*; D003080:Cold Temperature; D003574:Cytochrome c Group / Q000378:metabolism*; D003600:Cytosol / Q000378:metabolism*; D053938:DNA Fragmentation / Q000502:physiology*; D008297:Male; D051379:Mice; D008928:Mitochondria / Q000378:metabolism*
D003574:Cytochrome c Group