Abstract
BACKGROUND: Copper plays an important role in the human body and is potentially related to the development of diabetes. The mechanism of copper death gene regulating immune infiltration in diabetes has not been studied. METHODS: Download microarray data from healthy normal and diabetic patients from the GEO database. The identification of differentially expressed genes (DEGs) was analyzed by gene enrichment. Using String online database and Cytoscape software to interact with the protein interaction network and make visual analysis. Using Wilcox analyze the correlation between the copoer death gene and diabetic mellitus. Analysis of the correlation between immune penetration cells and functions, and the difference between the diabetes group and the control group, screening the copper death gene associated with diabetes, and predicting the upper top of microRNA (miRNA) through the Funrich software. RESULTS: According to the identification of differential genes in 25 samples of GSE25724 and GSE95849 data sets, 328 differential genes were identified by consensus, including 190 up-regulated genes and 138 down-regulated genes (log2FC = 2, P < .01). KEGG results showed that neurodegeneration-multiple disease pathways were most significantly upregulated, followed by Huntington disease. According to Cytohubba, the TOP10 genes HCK, FPR1, MNDA, AQP9, TLR8, CXCR1, CSF3R, VNN2, TLR4, and CCR5 are down-regulated genes, which are mostly enriched in neutrophils. Immunoinfiltration-related heat maps show that Macrophage was strongly positively correlated with Activated dendritic cell, Mast cell, Neutrophil, and Regulatory T cell showed a strong positive correlation. Neutrophil was strongly positively correlated with Activated dendritic cell, Mast cell, and Regulatory T cell. Differential analysis of immune infiltration showed that Neutroph, Mast cell, Activated B cell, Macrophage and Eosinophil were significantly increased in the diabetic group. Central memory CD4 T cell (P < .001), Plasmacytoid dendritic cell, Immature dendritic cell, and Central memory CD8 T cell, etal were significantly decreased. DBT, SLC31A1, ATP7A, LIAS, ATP7B, PDHA1, DLST, PDHB, GCSH, LIPT1, DLD, FDX1, and DLAT genes were significantly associated with one or more cells and their functions in immune invasion. Forty-one miRNA. CONCLUSIONS: Copper death is closely related to the occurrence of diabetes. Copper death genes may play an important role in the immune infiltration of diabetes.