Expression data from rat brain following ischemic stroke or undercut

Despite well-known risk factors such as stroke and head trauma, it has not been clinically effective to prevent acquired epilepsy. To do so, it is crucial to understand what commonly drives neural hyperexcitability. Using comparative transcriptome analyses with different models of acquired epilepsy including stroke and head trauma (the present GEO case), as well as blood-brain barrier (BBB) disruption, albumin, and TGFβ application (GEO accession number: GSE12304), we show that TGFβ signaling activation following BBB disruption commonly occurs regardless of brain region and insult types, accompanied by the strong upregulation of genes relevant to inflammation and extracellular matrix (ECM) modulation.尽管中风、颅脑创伤等已是公认的获得性癫痫(acquired epilepsy)高危风险因素，但目前临床上仍无法实现获得性癫痫的有效预防。要达成这一防控目标，明确神经兴奋性亢进(neural hyperexcitability)的常见驱动机制至关重要。本研究针对多种获得性癫痫模型开展比较转录组分析，涵盖中风、颅脑创伤(本研究的基因表达综合数据库(Gene Expression Omnibus, GEO)数据集)，以及血脑屏障(blood-brain barrier, BBB)破坏、白蛋白处理与转化生长因子β(transforming growth factor β, TGFβ)处理模型(GEO登录号：GSE12304)。研究结果表明，血脑屏障破坏后触发的TGFβ信号通路激活普遍存在于不同脑区与损伤类型中，同时伴随炎症相关基因与细胞外基质(extracellular matrix, ECM)调控相关基因的显著上调。