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免疫性血小板减少症（ITP）和癫痫之间可能存在共同的生物学途径，即血管生成和 MAPK 通路的负调控。

Negative regulation of angiogenesis and the MAPK pathway may be a shared biological pathway between IS and epilepsy.

机构信息

Department of Neurourgery, Second Affiliated Hospital of Xi'an Jiao Tong University, Xi'an, China.

Department of Thoracic Surgery, Second Affiliated Hospital of Xi'an Jiao Tong University, Xi'an, China.

出版信息

PLoS One. 2023 Oct 4;18(10):e0286426. doi: 10.1371/journal.pone.0286426. eCollection 2023.

DOI:10.1371/journal.pone.0286426
PMID:37792772
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10550183/
Abstract

Ischemia stroke and epilepsy are two neurological diseases that have significant patient and societal burden, with similar symptoms of neurological deficits. However, the underlying mechanism of their co-morbidity are still unclear. In this study, we performed a combined analysis of six gene expression profiles (GSE58294, GSE22255, GSE143272, GSE88723, GSE163654, and GSE174574) to reveal the common mechanisms of IS and epilepsy. In the mouse datasets, 74 genes were co-upregulated and 7 genes were co-downregulated in the stroke and epilepsy groups. Further analysis revealed that the co-expressed differentially expressed genes (DEGs) were involved in negative regulation of angiogenesis and the MAPK signaling pathway, and this was verified by Gene Set Enrichment Analysis of human datasets and single cell RNA sequence of middle cerebral artery occlusion mice. In addition, combining DEGs of human and mouse, PTGS2, TMCC3, KCNJ2, and GADD45B were identified as cross species conserved hub genes. Meanwhile, molecular docking results revealed that trichostatin A and valproic acid may be potential therapeutic drugs. In conclusion, to our best knowledge, this study conducted the first comorbidity analysis of epilepsy and ischemic stroke to identify the potential common pathogenic mechanisms and drugs. The findings may provide an important reference for the further studies on post-stroke epilepsy.

摘要

缺血性脑卒中与癫痫是两种具有显著患者和社会负担的神经疾病，具有相似的神经功能缺损症状。然而，它们合并存在的潜在机制仍不清楚。在这项研究中，我们对六个基因表达谱（GSE58294、GSE22255、GSE143272、GSE88723、GSE163654 和 GSE174574）进行了联合分析，以揭示 IS 和癫痫的共同机制。在小鼠数据集，脑卒中组和癫痫组有 74 个基因共上调，7 个基因共下调。进一步分析显示，共同表达的差异表达基因（DEGs）参与了血管生成和 MAPK 信号通路的负调控，这通过对人类数据集的基因集富集分析和大脑中动脉闭塞小鼠的单细胞 RNA 序列得到了验证。此外，将人类和小鼠的 DEGs 相结合，PTGS2、TMCC3、KCNJ2 和 GADD45B 被鉴定为跨物种保守的枢纽基因。同时，分子对接结果表明曲古抑菌素 A 和丙戊酸可能是潜在的治疗药物。总之，据我们所知，这项研究首次对癫痫和缺血性脑卒中的合并症进行了分析，以确定潜在的共同发病机制和药物。这些发现可能为脑卒中后癫痫的进一步研究提供重要参考。

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