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TNF-alpha and phosphorylation of ERK in DRG and spinal cord: insights into mechanisms of sciatica.

机译：DRG和脊髓中的TNF-α和ERK磷酸化：坐骨神经痛机理的见解。

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STUDY DESIGN: Characterize extracellular signal-regulated kinase (ERK) and its phosphorylation (pERK) in neural tissues after topical application of tumor necrosis factor-alpha (TNF-alpha) to L5 nerve root. OBJECTIVE: Identify time-course, localization, and expression of pERK. SUMMARY OF BACKGROUND DATA: TNF-alpha has a key role in disc herniation and sciatica as an inflammatory component of the nucleus pulposus. ERK is associated with neuronal signal transduction and nociception. METHODS: We studied tissue from naive rats, vehicle-treated rats, and rats receiving rat recombinant TNF-alpha using Western blots of total and phosphorylated ERK (pERK). We used immunohistochemistry of pERK with neuronal nuclear (NeuN) antibody to identify its cellular distribution. RESULTS: Topical application of TNF-alpha to rat nerve root increased pERK in ipsilateral dorsal root ganglion (DRG) neurons and glia within 5 hours. pERK was not expressed in DRG during the first hour after TNF-alpha application, nor was it seenat anytime in spinal cord dorsal horn. DRG satellite cells had increased pERK 5 hours after TNF-alpha or vehicle treatment. TNF-alpha treatment increased pERK in small- and medium-sized DRG neurons and to a lesser degree in large neurons. CONCLUSIONS: These findings suggest that ERK signaling plays a role in the activation of DRG cells following inflammatory injuries to nerve roots and further documents the importance of inflammation in the pathogenesis of painful spine disorders.
机译：研究设计：将肿瘤坏死因子-α（TNF-alpha）局部应用到L5神经根后，表征神经组织中的细胞外信号调节激酶（ERK）及其磷酸化（pERK）。目的：确定pERK的时程，定位和表达。背景数据概述：TNF-α在椎间盘突出症和坐骨神经痛中作为髓核的炎性成分具有关键作用。 ERK与神经元信号转导和伤害感受有关。方法：我们使用总ERK和磷酸化ERK（pERK）的蛋白质印迹研究了来自幼稚大鼠，媒介物治疗大鼠和接受大鼠重组TNF-α的大鼠的组织。我们使用pERK的免疫组化与神经元核（NeuN）抗体来鉴定其细胞分布。结果：在大鼠神经根局部应用TNF-α可以在5小时内增加同侧背根神经节（DRG）神经元和神经胶质中的pERK。在施用TNF-α后的第一小时内，DRG中没有表达pERK，也没有在脊髓背角中任何时候看到它。 TNF-α或媒介物处理5小时后，DRG卫星细胞的pERK增加。 TNF-α治疗在中小型DRG神经元中增加pERK，而在大型神经元中增加程度较小。结论：这些发现表明ERK信号传导在神经根发炎性损伤后在DRG细胞的活化中起作用，并且进一步证明了炎症在疼痛性脊柱疾病的发病机理中的重要性。

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