Abstract
Cardiac-cerebral vascular disease (CCVD), is primarily induced by atherosclerosis, and is a leading cause of mortality. Numerous studies have investigated and attempted to clarify the molecular mechanisms of atherosclerosis; however, its pathogenesis has yet to be completely elucidated. Two expression profiling datasets, GSE43292 and GSE57691, were obtained from the Gene Expression Omnibus (GEO) database. The present study then identified the differentially expressed genes (DEGs), and functional annotation of the DEGs was performed. Finally, an atherosclerosis animal model and neural network prediction model was constructed to verify the relationship between hub gene and atherosclerosis. The results identified a total of 234 DEGs between the normal and atherosclerosis samples. The DEGs were mainly enriched in actin filament, actin binding, smooth muscle cells, and cytokine-cytokine receptor interactions. A total of 13 genes were identified as hub genes. Following verification of animal model, the common DEG, Tropomyosin 2 (TPM2), was found, which were displayed at lower levels in the atherosclerosis models and samples. In summary, DEGs identified in the present study may assist clinicians in understanding the pathogenesis governing the occurrence and development of atherosclerosis, and TPM2 exhibits potential as a promising diagnostic and therapeutic biomarker for atherosclerosis.
Highlights
Cardiac-cerebral vascular diseases (CCVDs) have a high prevalence, disability and mortality rates, and are a serious threat to human health, especially to the health of the populace aged over 50 years [1]
15 million people die from CCVDs, which are primarily induced by atherosclerosis, and are the leading cause of mortality in the world [2]
Numerous studies [3,4,5,6,7] have demonstrated that the pathophysiological process for the development of atherosclerosis are closely associated with the mutation and abnormal expression of genes, which include fms-like tyrosine kinase-1 (Flt-1), tumor necrosis factor (TNF)-α, apolipoprotein A-I, vascular endothelial growth factor (VEGF) and angiogenin
Summary
Cardiac-cerebral vascular diseases (CCVDs) have a high prevalence, disability and mortality rates, and are a serious threat to human health, especially to the health of the populace aged over 50 years [1]. Numerous studies [3,4,5,6,7] have demonstrated that the pathophysiological process for the development of atherosclerosis are closely associated with the mutation and abnormal expression of genes, which include fms-like tyrosine kinase-1 (Flt-1), tumor necrosis factor (TNF)-α, apolipoprotein A-I (apoA-I), vascular endothelial growth factor (VEGF) and angiogenin. The molecular mechanisms of the occurrence and development of atherosclerosis were subsequently explored via enrichment analysis of functions and pathways, protein-protein interaction (PPI) network analyses and co-expression network analyses, and a total of 234 DEGs and 13 hub genes were identified and authenticated. After comparing the bioinformatics result and proteomic data, Tropomyosin 2 (TPM2) was identified as a commonly differentially expressed gene, which exhibits potential as a molecular target or biomarker for atherosclerosis. A series of low flux experiments were subsequently performed to verify the role and function of TPM2 in atherosclerosis
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