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首页> 外文期刊>Neuropharmacology >Cell-specific role for epsilon- and betaI-protein kinase C isozymes in protecting cortical neurons and astrocytes from ischemia-like injury.
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Cell-specific role for epsilon- and betaI-protein kinase C isozymes in protecting cortical neurons and astrocytes from ischemia-like injury.

机译：ε和βI蛋白激酶C同工酶在保护皮质神经元和星形胶质细胞免受缺血样损伤中的细胞特异性作用。

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Activation of epsilon protein kinase C (epsilonPKC) has been shown to protect cardiac myocytes against ischemia and reperfusion injury. However, the role of PKC in ischemic brain injury is less well defined. Western blot analysis of murine neurons and astrocytes in primary culture demonstrated epsilon- and betaIPKC expression in both cell types. Activation of epsilonPKC increased in neuronal cultures in response to the ischemia-like insult of oxygen-glucose deprivation (OGD). Isozyme-specific peptide activators or inhibitors of PKC were applied at various times before, during and after the OGD period. Neuron-astrocyte mixed cultures pretreated with a selective epsilonPKC activator peptide showed a significant reduction in neuronal injury after OGD and reperfusion, compared to cultures pretreated with control peptide. The epsilonPKC activator peptide counteracted the increased damage induced by pretreatment with the epsilonPKC-selective inhibitor peptide in relatively pure neuronal cultures subjected toOGD. Neither epsilonPKC activator nor inhibitor peptides affected injury of neurons when applied after OGD onset. In contrast, the betaIPKC-selective inhibitor peptide increased injury in astrocyte cultures exposed to OGD at all application times tested. Our data demonstrate protection of neurons by selective activation of epsilonPKC but enhanced astrocyte cell death with selective inhibition of betaIPKC. Thus PKC isozymes exhibit cell type-specific effects on ischemia-like injury.
机译：ε蛋白激酶C（epsilonPKC）的激活已显示可以保护心肌细胞免受缺血和再灌注损伤。但是，PKC在缺血性脑损伤中的作用尚不清楚。在原代培养中的鼠神经元和星形胶质细胞的蛋白质印迹分析表明，两种细胞类型中都有ε和betaIPKC表达。响应缺血样的氧葡萄糖剥夺（OGD）损伤，神经元培养物中epsilonPKC的激活增加。在OGD期之前，期间和之后的不同时间使用同工酶特异性肽激活剂或PKC抑制剂。与用对照肽预处理的培养物相比，用选择性epsilonPKC激活剂肽预处理的神经元-星形细胞混合培养物显示OGD和再灌注后神经元损伤显着减少。在经受OGD的相对纯的神经元培养物中，epsilonPKC激活剂肽抵消了通过用epsilonPKC选择性抑制剂肽预处理诱导的增加的损伤。 OGD发作后使用时，epsilonPKC激活剂和抑制剂肽都不会影响神经元的损伤。相反，在测试的所有施用时间，暴露于OGD的星形胶质细胞培养物中，βIPKC-选择性抑制剂肽会增加损伤。我们的数据表明，通过选择性激活epsilonPKC可以保护神经元，但通过选择性抑制betaIPKC可以增强星形胶质细胞的死亡。因此，PKC同工酶对缺血样损伤表现出细胞类型特异性作用。

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