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首页> 外文期刊>BMC Neuroscience >PKCε phosphorylation regulates the mitochondrial translocation of ATF2 in ischemia-induced neurodegeneration
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PKCε phosphorylation regulates the mitochondrial translocation of ATF2 in ischemia-induced neurodegeneration

机译：PKCε磷酸化调节缺血性神经变性中ATF2的线粒体易位

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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. 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. Our results support the hypothesis that PKCε regulates phosphorylation and nuclear sequestration of ATF2 in hippocampal neurons during ischemia-induced neurodegeneration.
机译：整体性脑缺血触发海马CA1区神经变性，但神经元死亡的机制仍然难以捉摸。最近发现蛋白激酶C（PKCε）的ε同工型是控制ATF2的核质运输和黑素瘤细胞存活的主要开关。评估PKCε–ATF2信号在神经变性中的作用很重要。在PKCε无效小鼠的海马中，Thr-52处ATF2的磷酸化降低，表明ATF2是PKCε的磷酸化底物。短暂性全脑缺血后4、24、48和72小时，PKCε蛋白浓度显着降低，导致核ATF2易位至线粒体。用Fluoro-Jade C阳性染色的退化神经元表现出细胞质ATF2。我们的研究结果支持以下假设：PKCε在缺血性神经变性期间调节海马神经元中ATF2的磷酸化和核螯合。

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