The Journal of Neuroscience, July 26, 2006, ():
Mitochondrial Translocation of p53 Mediates Release of Cytochrome c and Hippocampal CA1 Neuronal Death after Transient Global Cerebral Ischemia in Rats
J. Neurosci. Endo et al.
26: 7974
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Supplemental Figure. Decreased mitochondrial p53 translocation after tGCI in copper-zinc superoxide dismutase (SOD1) transgenic (Tg) rats. A, Western blot analysis of p53 in the mitochondrial fraction from the hippocampal CA1 subregion 8 h after tGCI. Mitochondrial p53 expression significantly decreased in the SOD1 Tg rats compared with wild-type (Wt) rats (n = 4, *p = 0.0039). B, Representative photomicrographs of fluorescent double staining of p53 (green) and hydroethidine (HEt) (red) in the hippocampal CA1 subregion 8 h after tGCI. Nuclei were counterstained with DAPI (blue). A strong cytosolic p53 expression was observed in the Wt rats. HEt is diffusible into the central nervous system parenchyma after an intravenous injection and is selectively oxidized to ethidium by superoxide anion, the production of which was shown by oxidized HEt signals in the cytosol of CA1 neurons in the Wt rats. An overlapped image shows that p53 expression and HEt signals colocalized in the Wt rats, however, signals of p53 and HEt were decreased in the SOD1 Tg rats. Scale bar, 20 μm.
