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ABS20200407_0001
| Genomics/Proteomics | |
| Potential Genes and Pathways Along with Immune Cells Infiltration in the Progression of Atherosclerosis Identified via Microarray Gene Expression Dataset Re-analysis | |
| Jing Xu1 | |
| Fuwai Hospital, China1 | |
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Background:
Atherosclerosis still remains the most common leading cause of ischemic heart disease and stroke, accounting for one-fourth deaths all around the world. Atherosclerosis was used to considered to be a result of chronic lipid build-up in the vessel wall. However, the pathogenesis of atherosclerosis is much more complex as knowledge progressed tremendously over the past decades, with a significant role for immune cells and inflammation in conjunction with hyperlipidemia, and the mechanisms and pathways mediating immune cells gradually dominate one of the trend in the study of atherosclerosis. No data-based studies have been conducted to analyze the potential genes and immune cells infiltration in the different stages of atherosclerosis, and it is of utmost importance to identify potential therapeutic targets to prevent or stabilize the disease process.
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Methods:
In this study, we downloaded GSE100927 and GSE28829 from NCBI-GEO database. Gene ontology and pathway enrichment were performed via DAVID database. The protein interaction network was constructed via STRING. Enriched hub genes were analyzed by Cytoscape software. The evaluation of the infiltrating immune cells in the dataset samples was performed by CIBERSORT algorithm.
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Results:
We identified 114 common upregulated differentially expressed genes (DEGs) and 22 common downregulated DEGs. (adjust p value < 0.01and log FC ¡Ã1). A cluster of 10 genes including CYBA, SLC11A1, FCER1G, ITGAM, ITGB2, CD53, ITGAX, VAMP8, CLEC5A and CD300A were found to be significant. Through the deconvolution algorithm CIBERSORT, we analyzed the significant alteration of immune cells infiltration in the progression of atherosclerosis with the threshold of Wilcoxon test at p value£¼0.05.
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Conclusion:
New strategies are needed for the prevention and treatment of atherosclerosis, including drugs that ideally reduce inflammation in the vessel wall without affecting host defense ability or tumor surveillance. The development of such therapies is challenging due to the complexity of atherosclerosis and the dynamic interactions that occur between the alterative infiltration of immune cells. Our study may help to identify potential therapeutic targets to prevent or stabilize the disease process.
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