文章摘要
王彬 ,吴炼铧 ,刘小平 ,刘垚 ,周娅 ,邓俊勇 ,邓发伟 ,胡东霞.脊髓损伤后痉挛相关基因的生物信息学分析[J].神经损伤功能重建,2023,(6):320-324
脊髓损伤后痉挛相关基因的生物信息学分析
Bioinformatics Analysis of Spasticity-related Genes after Spinal Cord Injur
  
DOI:
中文关键词: 脊髓损伤  痉挛  生物信息学  机制
英文关键词: spinal cord injury  spasticity  bioinformatics  mechanism
基金项目:江西省中医药管理 局 科 技 计 划 项 目 (No. 2021Z018)
作者单位
王彬1 ,吴炼铧1 ,刘小平1 ,刘垚2 ,周娅2 ,邓俊勇1 ,邓发伟1 ,胡东霞1 1. 南昌大学第二附 属 医 院 康 复 医 学 科 2. 昆明医科大学康 复学院 
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中文摘要:
      目的:对大鼠脊髓损伤(SCI)后痉挛相关基因进行生物信息学分析,探索SCI后痉挛发生的分子机 制。方法:在GEO数据库下载SCI后痉挛的基因表达谱芯片数据GSE16710,采用在线工具GEO 2R筛选差 异表达基因(DEG),筛选标准为P<0.05及|log2FC|≥1,通过火山图进行可视化;使用DAVID数据库对筛 选的DEG进行GO功能富集和KEGG通路分析,使用ImageGP可视化;通过STRING数据库构建DEGs的 蛋白-蛋白互作(PPI)网络分析,利用Cytoscape软件进行可视化,并运用CytoHubba插件和DEPs的degree 值筛选PPI网络中前10位的关键基因。结果:总共筛选得到313个DEGs,其中有92个上调基因和221个下 调基因;GO富集分析结果发现DEGs主要集中在谷氨酸能突触传递的调节、突触传递的正向调节、神经元 投射发展的调节及磷脂酰肌醇-3激酶信号等生物学过程上;KEGG通路分析表明,DEGs主要富集在长时 程增强、谷氨酸能突触、MAPK 信号途径及 cAMP 信号途径等通路上;PPI 分析发现,Mapt、Gad1、Gria2、 Fmr1、Reln、Mbp及Cav1等前10位是关键基因。结论:通过生信工具分析了SCI后痉挛中的关键DEGs和 通路,帮助理解其分子机制及在痉挛发生、发展过程中的作用,为该病的治疗提供了理论依据。
英文摘要:
      To perform bioinformatics analysis on spasticity-related genes after spinal cord injury (SCI) in rats, and explore the molecular mechanisms underlying spasticity after SCI. Methods: GSE16710, the gene expression profile chip data related to spasticity after SCI, were downloaded from the GEO database. Differentially expressed genes (DEGs) were identified using the online tool GEO 2R based on the screening criteria of P<0.05 and |log2FC|≥1, and visualized using volcano maps. The identified DEGs were subjected to GO functional enrichment and KEGG pathway analyses using the DAVID database, and the results were visualized using ImageGP. Protein-protein interaction (PPI) network analysis of DEGs was constructed using the STRING database and visualized using Cytoscape software; the top 10 key genes in the PPI networks were selected using the CytoHubba plugin and the degree values of differentially expressed proteins (DEPs). Results: A total of 313 DEGs were identified, of which 92 were upregulated genes and 221 were downregulated genes. GO enrichment analysis showed that the DEGs were mainly involved in biological processes such as the regulation of glutamatergic synaptic transmission, positive regulation of synaptic transmission, regulation of neuronal projection development, and regulation of phosphatidylinositol 3-kinase signaling. KEGG pathway analysis revealed that the DEGs were mainly enriched in long-term potentiation, glutamatergic synapse, MAPK signaling pathway, and cAMP signaling pathway. PPI analysis identified the top 10 key genes, including Mapt, Gad1, Gria2, Fmr1, Reln, Mbp, and Cav1. Conclusion: Through bioinformatics analysis of key DEGs and pathways involved in spasticity after SCI, this study provides insights into the underlying molecular mechanisms and their roles in the occurrence and development of spasticity, thus providing a theoretical basis for the treatment of this disease.
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