Identification of the key genes associated with neuropathic pain

Abstract

Neuropathic pain is a chronic pain state associated with multiple etiologies that results in considerable social and economic burden. The identification of key genes associated with neuropathic pain is important for the development of novel therapies. Therefore, the present study downloaded the gene expression profile GSE15041 from the Gene Expression Omnibus database. The unverified gene chip was removed and the microarray data was normalized following quality control. The limma package in R was used to screen the differentially expressed genes (DEGs), followed by Gene Ontology and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis. Furthermore, a protein-protein interaction (PPI) network based on the identified DEGs was constructed to select hub proteins, and reverse transcription-quantitative polymerase chain reaction was performed to detect the expression of these proteins in a mouse model of neuropathic pain. In total, 86 common DEGs were identified. DEGs were significantly enriched in ‘extracellular space’ and KEGG pathway enrichment analysis demonstrated that the DEGs were significantly enriched in inflammatory diseases and the mitogen-activated protein kinase signaling pathway. The PPI network consisted of 27 nodes (proteins) and 47 PPI edges (interactions). Interleukin (IL)-6, transcription factor AP-1 (c-Jun) and urikinase-type plasminogen activator (Plau) were identified as hub proteins and key genes in neuropathic pain. The mRNA expression of these hub proteins was significantly increased in the neuropathic pain model, compared with the sham group. IL-6, c-Jun, and Plau may be involved in development of neuropathic pain and further research investigating the exact role of these key genes is required.

Crotoxin Conjugated to SBA-15 Nanostructured Mesoporous Silica Induces Long-Last Analgesic Effect in the Neuropathic Pain Model in Mice

“…Increased activity and number of glial cells may contribute to neuropathic pain, since activation of glial cells due to neuropathy observed after peripheral nerve damage leads to the release of cytokines, such as TNF-α, IL-6, IL-10, and IL-1β and chemokines at the CNS [50,51], which can modulate inflammatory response and nociceptive transmission [1,52]. Interleukins contribute to cortical mechanisms of sensitization [1], and in particular IL-6 may have an important role in the development and maintenance of pathological pain, such as neuropathic pain [53,54]. Neuropathic models, including PSNL, have been shown to enhance expression of IL-6 in the spinal cord and dorsal root ganglia [55,56].…”

Identification of candidate genes and miRNAs associated with neuropathic pain induced by spared nerve injury

“…Microarray profiling was previously used to explore the altered gene expression of the murine nervous system following nerve injury (10,11). This led to the identification of IL-6 , c-Jun and Plau as crucial genes (12) and DNA binding, cell cycle, and forkhead box protein as a major signaling pathway involved in NP (13). Despite these investigations profiling post nerve injury gene expression using microarray analysis, NP's pathological mechanisms remain poorly understood.…”

Analyses of gene expression profiles in the rat dorsal horn of the spinal cord using RNA sequencing in chronic constriction injury rats

“…Gene expression profile studies can be used to provide understanding of the molecular mechanisms underlying the development and maintenance of neuropathic pain [ 10 – 12 ]. Some studies using microarray and RNA sequencing (RNA-seq) analysis have been conducted to investigate the mechanism underlying the generation of neuropathic pain in spared nerve injury (SNI) model [ 13 , 14 ].…”