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Background

Global cerebral ischemia triggers neurodegeneration in the hippocampal CA1 region, but the mechanism of neuronal death remains elusive. The epsilon isoform of protein kinase C (PKCε) has recently been identified as a master switch that controls the nucleocytoplasmic trafficking of ATF2 and the survival of melanoma cells. It is of interest to assess the role of PKCε-ATF2 signaling in neurodegeneration.

Results

Phosphorylation of ATF2 at Thr-52 was reduced in the hippocampus of PKCε null mice, suggesting that ATF2 is a phosphorylation substrate of PKCε. PKCε protein concentrations were significantly reduced 4, 24, 48 and 72 h after transient global cerebral ischemia, resulting in translocation of nuclear ATF2 to the mitochondria. Degenerating neurons staining positively with Fluoro-Jade C exhibited cytoplasmic ATF2.

Conclusions

Our results support the hypothesis that PKCε regulates phosphorylation and nuclear sequestration of ATF2 in hippocampal neurons during ischemia-induced neurodegeneration."xsd:string
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http://purl.uniprot.org/citations/30497386http://purl.uniprot.org/core/author"Kumar V."xsd:string
http://purl.uniprot.org/citations/30497386http://purl.uniprot.org/core/author"Wu Y.C."xsd:string
http://purl.uniprot.org/citations/30497386http://purl.uniprot.org/core/author"Weng Y.C."xsd:string
http://purl.uniprot.org/citations/30497386http://purl.uniprot.org/core/author"Chou W.H."xsd:string
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