Identification of the common differentially expressed genes and pathogenesis between neuropathic pain and aging

Qingqing Ye; Zhensheng Huang; Weicheng Lu; Fang Yan; Weian Zeng; Jingdun Xie; Weiqiang Zhong

doi:10.3389/fnins.2022.994575

Identification of the common differentially expressed genes and pathogenesis between neuropathic pain and aging

Front Neurosci. 2022 Oct 19:16:994575. doi: 10.3389/fnins.2022.994575. eCollection 2022.

Authors

Qingqing Ye¹, Zhensheng Huang¹, Weicheng Lu¹, Fang Yan¹, Weian Zeng¹, Jingdun Xie¹, Weiqiang Zhong¹

Affiliation

¹ State Key Laboratory of Oncology in Southern China, Department of Anesthesiology, Collaborative Innovation for Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, China.

Abstract

Background: Neuropathic pain is a debilitating disease caused by damage or diseases of the somatosensory nervous system. Previous research has indicated potential associations between neuropathic pain and aging. However, the mechanisms by which they are interconnected remain unclear. In this study, we aim to identify the common differentially expressed genes (co-DEGs) between neuropathic pain and aging through integrated bioinformatics methods and further explore the underlying molecular mechanisms.

Methods: The microarray datasets GSE24982, GSE63442, and GSE63651 were downloaded from Gene Expression Omnibus (GEO) database. Differentially expressed genes (DEGs) and co-DEGs were first identified. Functional enrichment analyses, protein-protein Interaction (PPI) network, module construction and hub genes identification were performed. Immune infiltration analysis was conducted. Targeted transcription factors (TFs), microRNAs (miRNAs) and potential effective drug compounds for hub genes were also predicted.

Results: A total of 563 and 1,250 DEGs of neuropathic pain and aging were screened, respectively. 16 genes were further identified as co-DEGs. The functional analysis emphasizes the vital roles of the humoral immune response and complement and coagulation cascades in these two diseases. Cxcl14, Fblim1, RT1-Da, Serping1, Cfd, and Fcgr2b were identified as hub genes. Activated B cell, mast cell, activated dendritic cell, CD56 bright natural killer cell, effector memory CD8 + T cell, and type 2 T helper cell were significantly up-regulated in the pain and aging condition. Importantly, hub genes were found to correlate with the activated B cell, activated dendritic cell, Gamma delta T cell, central memory CD4 + T cell and mast cell in pain and aging diseases. Finally, Spic, miR-883-5p, and miR-363-5p et al. were predicted as the potential vital regulators for hub genes. Aldesleukin, Valziflocept, MGD-010, Cinryze, and Rhucin were the potential effective drugs in neuropathic pain and aging.

Conclusion: This study identified co-DEGs, revealed molecular mechanisms, demonstrated the immune microenvironment, and predicted the possible TFs, miRNAs regulation networks and new drug targets for neuropathic pain and aging, providing novel insights into further research.

Keywords: aging; co-DEGs; immune infiltration; neuropathic pain; regulation network.