Higher expression of PLEK and LY86 as the potential biomarker of carotid atherosclerosis

Abstract

Carotid atherosclerosis (AS) occurs in atherosclerotic lesions of the carotid artery, which can lead to transient ischemic attack and stroke in severe cases. However, the relationship between pleckstrin (PLEK) and lymphocyte antigen 86 (LY86) and carotid AS remains unclear. The carotid AS datasets GSE43292 and GSE125771 were downloaded from the gene expression omnibus database. Differentially expressed genes (DEGs) were screened and weighted gene co-expression network analysis was performed. Construction and analysis of protein-protein interaction network. Functional enrichment analysis, gene set enrichment analysis and comparative toxicogenomics database analysis were performed. TargetScan screened miRNAs that regulated central DEGs. A total of 305 DEGs were identified. According to gene ontology analysis, they were mainly enriched in immune system processes, extracellular regions and cytokine binding. Kyoto encyclopedia of genes and genomes analysis showed that the target cells were mainly enriched in Rap1 signal pathway, B cell receptor signal pathway and PPAR signal pathway. In the enrichment project of metascape, the reaction to bacteria, cell activation and chemotaxis can be seen in the enrichment project of gene ontology. Total 10 core genes (TYROBP, FCER1G, PLEK, LY86, IL10RA, ITGB2, LCP2, FCGR2B, CD86, CCR1) were obtained by protein-protein interaction network construction and analysis. Core genes (PLEK, LY86, IL10RA, ITGB2, and LCP2) were highly expressed in carotid AS samples and lowly expressed in normal samples. Comparative toxicogenomics database analysis showed that 5 genes were associated with pneumonia, inflammation, necrosis, and drug allergy. PLEK and LY86 genes are highly expressed in carotid AS. The higher the expression of PLEK and LY86, the worse the prognosis is.