scholarly journals Bioinformatics Analyses of Differentially Expressed Genes Associated with Acute Myocardial Infarction

2016 ◽  
Vol 34 (2) ◽  
pp. 67-75 ◽  
Author(s):  
Yuan Gao ◽  
Guo-xian Qi ◽  
Liang Guo ◽  
Ying-xian Sun
2019 ◽  
Vol 2019 ◽  
pp. 1-11 ◽  
Author(s):  
Yan Li ◽  
Xiao_nan He ◽  
Chao Li ◽  
Ling Gong ◽  
Min Liu

Background. Identification of potential molecular targets of acute myocardial infarction is crucial to our comprehensive understanding of the disease mechanism. However, studies of gene coexpression analysis via jointing multiple microarray data of acute myocardial infarction still remain restricted. Methods. Microarray data of acute myocardial infarction (GSE48060, GSE66360, GSE97320, and GSE19339) were downloaded from Gene Expression Omnibus database. Three data sets without heterogeneity (GSE48060, GSE66360, and GSE97320) were subjected to differential expression analysis using MetaDE package. Differentially expressed genes having upper 25% variation across samples were imported in weighted gene coexpression network analysis. Functional and pathway enrichment analyses were conducted for genes in the most significant module using DAVID. The predicted microRNAs to regulate target genes in the most significant module were identified using TargetScan. Moreover, subpathway analyses using iSubpathwayMiner package and GenCLiP 2.0 were performed on hub genes with high connective weight in the most significant module. Results. A total of 1027 differentially expressed genes and 33 specific modules were screened out between acute myocardial infarction patients and control samples. Ficolin (collagen/fibrinogen domain containing) 1 (FCN1), CD14 molecule (CD14), S100 calcium binding protein A9 (S100A9), and mitochondrial aldehyde dehydrogenase 2 (ALDH2) were identified as critical target molecules; hsa-let-7d, hsa-let-7b, hsa-miR-124-3, and hsa-miR-9-1 were identified as potential regulators of the expression of the key genes in the two biggest modules. Conclusions. FCN1, CD14, S100A9, ALDH2, hsa-let-7d, hsa-let-7b, hsa-miR-124-3, and hsa-miR-9-1 were identified as potential candidate regulators in acute myocardial infarction. These findings might provide new comprehension into the underlying molecular mechanism of disease.


2021 ◽  
Vol 2021 ◽  
pp. 1-19
Author(s):  
Siyu Guo ◽  
Zhihong Huang ◽  
Xinkui Liu ◽  
Jingyuan Zhang ◽  
Peizhi Ye ◽  
...  

Acute coronary syndrome (ACS) is a complex syndrome of clinical symptoms. In order to accurately diagnose the type of disease in ACS patients, this study is aimed at exploring the differentially expressed genes (DEGs) and biological pathways between acute myocardial infarction (AMI) and unstable angina (UA). The GSE29111 and GSE60993 datasets containing microarray data from AMI and UA patients were downloaded from the Gene Expression Omnibus (GEO) database. DEG analysis of these 2 datasets is performed using the “limma” package in R software. DEGs were also analyzed using protein-protein interaction (PPI), Molecular Complex Detection (MCODE) algorithm, Gene Ontology (GO), and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis. Correlation analysis and “cytoHubba” were used to analyze the hub genes. A total of 286 DEGs were obtained from GSE29111 and GSE60993, including 132 upregulated genes and 154 downregulated genes. Subsequent comprehensive analysis identified 20 key genes that may be related to the occurrence and development of AMI and UA and were involved in the inflammatory response, interaction of neuroactive ligand-receptor, calcium signaling pathway, inflammatory mediator regulation of TRP channels, viral protein interaction with cytokine and cytokine receptor, human cytomegalovirus infection, and cytokine-cytokine receptor interaction pathway. The integrated bioinformatical analysis could improve our understanding of DEGs between AMI and UA. The results of this study might provide a new perspective and reference for the early diagnosis and treatment of ACS.


2019 ◽  
Vol 2019 ◽  
pp. 1-13 ◽  
Author(s):  
Da-Qiu Chen ◽  
Xiang-Sheng Kong ◽  
Xue-Bin Shen ◽  
Mao-Zhi Huang ◽  
Jian-Ping Zheng ◽  
...  

Background. Acute myocardial infarction (AMI) is a common disease with high morbidity and mortality around the world. The aim of this research was to determine the differentially expressed genes (DEGs), which may serve as potential therapeutic targets or new biomarkers in AMI. Methods. From the Gene Expression Omnibus (GEO) database, three gene expression profiles (GSE775, GSE19322, and GSE97494) were downloaded. To identify the DEGs, integrated bioinformatics analysis and robust rank aggregation (RRA) method were applied. These DEGs were performed through Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses by using Clusterprofiler package. In order to explore the correlation between these DEGs, the interaction network of protein-protein internet (PPI) was constructed using the STRING database. Utilizing the MCODE plug-in of Cytoscape, the module analysis was performed. Utilizing the cytoHubba plug-in, the hub genes were screened out. Results. 57 DEGs in total were identified, including 2 down- and 55 upregulated genes. These DEGs were mainly enriched in cytokine-cytokine receptor interaction, chemokine signaling pathway, TNF signaling pathway, and so on. The module analysis filtered out 18 key genes, including Cxcl5, Arg1, Cxcl1, Spp1, Selp, Ptx3, Tnfaip6, Mmp8, Serpine1, Ptgs2, Il6, Il1r2, Il1b, Ccl3, Ccr1, Hmox1, Cxcl2, and Ccl2. Ccr1 was the most fundamental gene in PPI network. 4 hub genes in total were identified, including Cxcl1, Cxcl2, Cxcl5, and Mmp8. Conclusion. This study may provide credible molecular biomarkers in terms of screening, diagnosis, and prognosis for AMI. Meanwhile, it also serves as a basis for exploring new therapeutic target for AMI.


2020 ◽  
Vol 2020 ◽  
pp. 1-10
Author(s):  
Xiaodong Sheng ◽  
Tao Fan ◽  
Xiaoqi Jin

Background. Acute myocardial infarction (AMI) is regarded as an urgent clinical entity, and identification of differentially expressed genes, lncRNAs, and altered pathways shall provide new insight into the molecular mechanisms behind AMI. Materials and Methods. Microarray data was collected to identify key genes and lncRNAs involved in AMI pathogenesis. The differential expression analysis and gene set enrichment analysis (GSEA) were employed to identify the upregulated and downregulated genes and pathways in AMI. The protein-protein interaction network and protein-RNA interaction analysis were utilized to reveal key long noncoding RNAs. Results. In the present study, we utilized gene expression profiles of circulating endothelial cells (CEC) from 49 patients of AMI and 50 controls and identified a total of 552 differentially expressed genes (DEGs). Based on these DEGs, we also observed that inflammatory response-related genes and pathways were highly upregulated in AMI. Mapping the DEGs to the protein-protein interaction (PPI) network and identifying the subnetworks, we found that OMD and WDFY3 were the hub nodes of two subnetworks with the highest connectivity, which were found to be involved in circadian rhythm and organ- or tissue-specific immune response. Furthermore, 23 lncRNAs were differentially expressed between AMI and control groups. Specifically, we identified some functional lncRNAs, including XIST and its antisense RNA, TSIX, and three lncRNAs (LINC00528, LINC00936, and LINC01001), which were predicted to be interacting with TLR2 and participate in Toll-like receptor signaling pathway. In addition, we also employed the MMPC algorithm to identify six gene signatures for AMI diagnosis. Particularly, the multivariable SVM model based on the six genes has achieved a satisfying performance ( AUC = 0.97 ). Conclusion. In conclusion, we have identified key regulatory lncRNAs implicated in AMI, which not only deepens our understanding of the lncRNA-related molecular mechanism of AMI but also provides computationally predicted regulatory lncRNAs for AMI researchers.


2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Giuliana Gobbi ◽  
Cecilia Carubbi ◽  
Guidantonio Malagoli Tagliazucchi ◽  
Elena Masselli ◽  
Prisco Mirandola ◽  
...  

AbstractAcute myocardial infarction is primarily due to coronary atherosclerotic plaque rupture and subsequent thrombus formation. Platelets play a key role in the genesis and progression of both atherosclerosis and thrombosis. Since platelets are anuclear cells that inherit their mRNA from megakaryocyte precursors and maintain it unchanged during their life span, gene expression profiling at the time of an acute myocardial infarction provides information concerning the platelet gene expression preceding the coronary event. In ST-segment elevation myocardial infarction (STEMI), a gene-by-gene analysis of the platelet gene expression identified five differentially expressed genes: FKBP5, S100P, SAMSN1, CLEC4E and S100A12. The logistic regression model used to combine the gene expression in a STEMI vs healthy donors score showed an AUC of 0.95. The same five differentially expressed genes were externally validated using platelet gene expression data from patients with coronary atherosclerosis but without thrombosis. Platelet gene expression profile highlights five genes able to identify STEMI patients and to discriminate them in the background of atherosclerosis. Consequently, early signals of an imminent acute myocardial infarction are likely to be found by platelet gene expression profiling before the infarction occurs.


2021 ◽  
Author(s):  
Hui Huang ◽  
Jiaxuan Zheng ◽  
Haiquan Tian ◽  
Yehan Fang ◽  
Wei Wang ◽  
...  

Abstract There are few studies on the genetic changes of meniscus degeneration. We used anterior cruciate ligament resection of Wuzhishan pig to prepare a meniscus degeneration model, and applied gene chip technology to detect differentially expressed genes in degenerative meniscus tissue. Then we applied GO analysis, Pathway analysis, Core gene network analysis and Relevant miRNAs analysis to discover relevant regulatory networks of meniscus degeneration. As a result, we detected 893 differentially expressed genes, mainly involving hormone, apoptosis, inflammation and other mechanisms, and obtained MUC13, Inflammatory mediator regulation of TRP channels, MDFI, mir-335-5p and so on that may play a key role. In summary, we have established a reliable animal model of meniscus degeneration and found that meniscus degeneration involves several possible molecular mechanisms, which will provide molecular targets for further research of the disease in the future.


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