Xuehui Zhang1, Naibin Yang2, Lijiang Shao3, Xuxia Chen3, Xueqin Chen4. 1. Department of General Practice, Ningbo First Hospital No. 59 Liuting Street, Haishu District, Ningbo, Zhejiang Province, P. R. China. 2. Department of Infectious Disease, Ningbo First Hospital No. 59 Liuting Street, Haishu District, Ningbo, Zhejiang Province, P. R. China. 3. Department of Emergency, Ningbo First Hospital No. 59 Liuting Street, Haishu District, Ningbo, Zhejiang Province, P. R. China. 4. Hospital Quality Management Office, Ningbo First Hospital No. 59 Liuting Street, Haishu District, Ningbo, Zhejiang Province, P. R. China.
Abstract
OBJECTIVE: The pathogenesis of pulmonary embolism (PE) remains unclear. This study was designed to determine the differential genes associated with PE autophagy via the gene expression omnibus (GEO). METHODS: Microarray data sets GSE11851 and GSE13535 were downloaded from the GEO to determine the differentially expressed genes (DEGs) of PE, and the protein-protein interaction (PPI) and hub gene networks were constructed by string and Cytoscape software. Additionally, the two data sets were screened to find the autophagy-related genes with common differential expression. Then, autophagy-related hub genes (ARHGs) overlapping with autophagy-related genes and hub genes were identified. Next, the mRNA-miRNA network was constructed, and finally the expressions of hub genes were determined with GSE11851 and GSE13535. RESULTS: A total of 235 common DEGs were identified, and C-C motif chemokine ligand 2 (CCL2) and MYC proto-oncogene (MYC) were identified to be the ARHGs of PE. Additionally, a co-expression network of mRNAs and miRNAs, consisting of 94 nodes and 103 edges, was constructed by Cytoscape. PE samples showed significantly higher expressions of CCL2 and MYC than the control samples (P < 0.05). According to gene set enrichment analysis (GSEA), CCL2 was closely correlated with oxidative stress and inflammatory reaction, while MYC was closely correlated with inflammatory reaction. CONCLUSION: According to analysis, CCL2 and MYC, with high expression in PE samples, are promising potential markers of PE. AJTR
OBJECTIVE: The pathogenesis of pulmonary embolism (PE) remains unclear. This study was designed to determine the differential genes associated with PE autophagy via the gene expression omnibus (GEO). METHODS: Microarray data sets GSE11851 and GSE13535 were downloaded from the GEO to determine the differentially expressed genes (DEGs) of PE, and the protein-protein interaction (PPI) and hub gene networks were constructed by string and Cytoscape software. Additionally, the two data sets were screened to find the autophagy-related genes with common differential expression. Then, autophagy-related hub genes (ARHGs) overlapping with autophagy-related genes and hub genes were identified. Next, the mRNA-miRNA network was constructed, and finally the expressions of hub genes were determined with GSE11851 and GSE13535. RESULTS: A total of 235 common DEGs were identified, and C-C motif chemokine ligand 2 (CCL2) and MYC proto-oncogene (MYC) were identified to be the ARHGs of PE. Additionally, a co-expression network of mRNAs and miRNAs, consisting of 94 nodes and 103 edges, was constructed by Cytoscape. PE samples showed significantly higher expressions of CCL2 and MYC than the control samples (P < 0.05). According to gene set enrichment analysis (GSEA), CCL2 was closely correlated with oxidative stress and inflammatory reaction, while MYC was closely correlated with inflammatory reaction. CONCLUSION: According to analysis, CCL2 and MYC, with high expression in PE samples, are promising potential markers of PE. AJTR
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