神经病理性疼痛
基因
SNi公司
医学
周围神经损伤
小桶
微阵列分析技术
微阵列
生物
神经损伤
信号转导
慢性疼痛
痛觉过敏
计算生物学
坐骨神经
痛觉超敏
生物信息学
背根神经节
坐骨神经损伤
神经科学
作者
Kai Wang,Duan Yi,Zhuoyin Yu,Bin Zhu,Shuiqing Li,Xiaoguang Liu
标识
DOI:10.3389/fnins.2020.00488
摘要
The reactivity enhancement of pain sensitive neurons in the nervous system is a feature of the pathogenesis for neuropathic pain (NP), yet the underlying mechanisms need to be fully understood. In this study, we made an attempt to clarify the NP-related hub genes and signaling pathways so as to provide effective diagnostic and therapeutic methods toward NP.Microarray expression profile GSE30691 including the mRNA-seq data of the spared nerve injury (SNI)-induced NP rats was accessed from the GEO database. Then, genes associated with NP development were screened using differential analysis along with random walk with restart (RWR). GO annotation and KEGG pathway analyses were performed to explore the biological functions and signaling pathways where the genes were activated. Afterward, protein-protein interaction (PPI) analysis and GO analysis were conducted to further identify the hub genes which showed an intimate correlation with NP development.Totally 94 genes associated with NP development were screened by differential analysis and RWR analysis, and they were observed to be predominantly enriched in hormone secretion and transport, cAMP signaling pathway and other NP occurrence associated functions and pathways. Thereafter, the 94 genes were subjected to PPI analysis to find the genes much more associated with NP and a functional module composed of 48 genes were obtained. 8 hub genes including C3, C1qb, Ccl2, Cxcl13, Timp1, Fcgr2b, Gal, and Lyz2 were eventually identified after further association and functional enrichment analyses, and the expression of these 8 genes were all higher in SNI rats by comparison with those in Sham rats.Based on the data collected from GEO database, this study discovered 8 hub genes that were closely related to NP occurrence and development, which help to provide potent theoretical basis for NP treatment.
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