Department of Musculoskeletal Biology, Institute of Ageing and Chronic Disease, University of Liverpool, Liverpool, UK.
Department of Molecular and Clinical Pharmacology, Institute of Translational Medicine, University of Liverpool, Liverpool, UK.
J Neurosci Res. 2019 Nov;97(11):1378-1392. doi: 10.1002/jnr.24441. Epub 2019 May 15.
Antiepileptogenic agents that prevent the development of epilepsy following a brain insult remain the holy grail of epilepsy therapeutics. We have employed a label-free proteomic approach that allows quantification of large numbers of brain-expressed proteins in a single analysis in the mouse (male C57BL/6J) kainate (KA) model of epileptogenesis. In addition, we have incorporated two putative antiepileptogenic drugs, postsynaptic density protein-95 blocking peptide (PSD95BP or Tat-NR2B9c) and a highly selective inducible nitric oxide synthase inhibitor, 1400W, to give an insight into how such agents might ameliorate epileptogenesis. The test drugs were administered after the induction of status epilepticus (SE) and the animals were euthanized at 7 days, their hippocampi removed, and subjected to LC-MS/MS analysis. A total of 2,579 proteins were identified; their normalized abundance was compared between treatment groups using ANOVA, with correction for multiple testing by false discovery rate. Significantly altered proteins were subjected to gene ontology and KEGG pathway enrichment analyses. KA-induced SE was most robustly associated with an alteration in the abundance of proteins involved in neuroinflammation, including heat shock protein beta-1 (HSP27), glial fibrillary acidic protein, and CD44 antigen. Treatment with PSD95BP or 1400W moderated the abundance of several of these proteins plus that of secretogranin and Src substrate cortactin. Pathway analysis identified the glutamatergic synapse as a key target for both drugs. Our observations require validation in a larger-scale investigation, with candidate proteins explored in more detail. Nevertheless, this study has identified several mechanisms by which epilepsy might develop and several targets for novel drug development. OPEN PRACTICES: This article has been awarded Open Data. All materials and data are publicly accessible as supporting information. Learn more about the Open Practices badges from the Center for Open Science: https://osf.io/tvyxz/wiki.
抗癫痫发作药物可预防脑损伤后癫痫的发生,这仍是癫痫治疗的圣杯。我们采用了一种无标签的蛋白质组学方法,可以在单次分析中定量检测大量在脑中表达的蛋白质,这种方法应用于癫痫发生的鼠(雄性 C57BL/6J)红藻氨酸(KA)模型中。此外,我们还加入了两种可能的抗癫痫发作药物,即突触后密度蛋白-95 阻断肽(PSD95BP 或 Tat-NR2B9c)和高度选择性诱导型一氧化氮合酶抑制剂 1400W,以深入了解这些药物如何改善癫痫发生。在诱导癫痫持续状态(SE)后给予测试药物,在 7 天时处死动物,取出其海马体,进行 LC-MS/MS 分析。共鉴定出 2579 种蛋白质;使用 ANOVA 比较治疗组之间的蛋白质归一化丰度,并通过假发现率对多重检验进行校正。对显著改变的蛋白质进行基因本体和 KEGG 通路富集分析。KA 诱导的 SE 与神经炎症相关的蛋白质丰度改变最密切相关,包括热休克蛋白β-1(HSP27)、神经胶质纤维酸性蛋白和 CD44 抗原。PSD95BP 或 1400W 治疗可调节其中几种蛋白质的丰度,以及分泌颗粒蛋白和Src 底物皮质蛋白的丰度。通路分析确定谷氨酸能突触是这两种药物的关键靶点。我们的观察结果需要在更大规模的研究中进行验证,并更详细地研究候选蛋白。尽管如此,这项研究已经确定了癫痫发生的几种机制和几种新药物开发的靶点。开放实践:本文已被授予开放数据。所有材料和数据均可公开访问,作为支持信息。从开放科学中心了解更多关于开放实践徽章的信息:https://osf.io/tvyxz/wiki。