TY - JOUR
T1 - Release of mitochondrial cytochrome c and DNA fragmentation after cold injury-induced brain trauma in mice
T2 - Possible role in neuronal apoptosis
AU - Morita-Fujimura, Yuiko
AU - Fujimura, Miki
AU - Kawase, Makoto
AU - Chen, Sylvia F.
AU - Chan, Pak H.
N1 - Funding Information:
This study was supported by National Institutes of Health grants NS14543, NS25372, NS36147, and contract NO1 NS82386. P.H.C. is a recipient of the Jacob Javits Neuroscience Investigator Award. We thank Cheryl Christensen for her editorial assistance and Liza Reola, Bernard Calagui and Jane O. Kim for their technical assistance.
PY - 1999/6/4
Y1 - 1999/6/4
N2 - 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.
AB - 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.
KW - Apoptosis
KW - Caspase
KW - Cold injury
KW - Cytochrome c
KW - Mitochondrial injury
KW - Traumatic brain injury
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U2 - 10.1016/S0304-3940(99)00327-4
DO - 10.1016/S0304-3940(99)00327-4
M3 - Article
C2 - 10381011
AN - SCOPUS:0033522851
VL - 267
SP - 201
EP - 205
JO - Neuroscience Letters
JF - Neuroscience Letters
SN - 0304-3940
IS - 3
ER -