Wu Zuolong. Screening and analyzing differentially expressed genes in rats after spinal cord injury[J]. Journal of Chongqing Medical University, 2021,46(10):1234-1241.
Wu Zuolong. Screening and analyzing differentially expressed genes in rats after spinal cord injury[J]. Journal of Chongqing Medical University, 2021,46(10):1234-1241. DOI: 10.13406/j.cnki.cyxb.002455.
Objective: To perform a bioinformatics analysis of the gene chip associated with spinal cord injury (SCI) in rats
so as to provide new ideas for clarifying the molecular mechanism of secondary SCI. Methods: Firstly
data sets GSE464 and GSE45006 of rat SCI mRNA expression profile were downloaded from the GEO database. The R language limma package was used to screen differential expression genes (DEGs) of injured and normal spinal cord and obtain the intersection. Then GO
KEGG and GSEA analyses were performed. Subsequently
the STRING online tool and Cytoscape software were used to construct and visualize a protein-protein interaction (PPI) network
and the cytoHubba plug-in was used to select the hub gene. Finally
the GOSemSim package was used to predict interactions between proteins encoded by the hub gene. Results: A total of 226 DEGs were screened. Functional annotation and pathway enrichment analysis showed that DEGs were mainly involved in biological processes (BP)
which contained response of cells to inflammation
regulation of ions
regeneration and repair; mainly participated in the main cellular components (CC) including presynaptic membrane
axonal ends and neuron projection endpoints; mediated the molecular function (MF): ATP phosphorylation
structural composition of the cytoskeleton
and binding to calcium-dependent proteins. Enriched pathways were mainly TNF
AGE-RAGE
NF-κB and Toll-like receptors. A total of 10 hub genes were obtained
namely Tubb5
Prkcd
Anxa2
Gns
Fabp5
Ctsc
Lyz2
Gusb
Vat1
and Grn
and were closely related with SCI. Among them
Prkcd
Ctsc
Vat1
Gns and Lyz2 genes in SCI lacked studies
and were worthy of further study. Conclusion: This study identifies hub genes and signaling pathways that may be involved in secondary SCI
and provides a new theoretical basis for the molecular mechanism of secondary SCI.