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Coronary Progenitor Cells and Soluble Biomarkers in Cardiovascular Prognosis after Coronary Angioplasty
Published on: January 28, 2020
Identification of biomarkers associated with phagocytosis regulatory factors in coronary artery disease using machine
Runan Jia1, Zhiya Li2, Yingying Du3
1Huaihe Hospital of Henan University, Kaifeng City, Henan, 475001, China. jrn950801@163.com.
Insights
Six biomarkers, including IL1B and TLR2, were identified for coronary artery disease (CAD) diagnosis. These findings enhance understanding of CAD pathogenesis and potential therapeutic strategies.
Area of Science:
- Biomedical research
- Genomics
- Immunology
Background:
- Coronary artery disease (CAD) is a leading global cause of mortality.
- Aberrant phagocytosis is implicated in CAD development.
- Identifying phagocytic regulatory factors offers potential for early CAD diagnosis.
Purpose of the Study:
- To identify novel biomarkers for coronary artery disease (CAD).
- To elucidate the role of phagocytic regulatory factors in CAD pathogenesis.
- To explore potential diagnostic and therapeutic strategies for CAD.
Main Methods:
- Analysis of Gene Expression Omnibus datasets (GSE66360, GSE113079, GSE59421).
- Identification of differentially expressed genes (DEGs) and co-expression network analysis.
- Machine learning algorithms, pathway enrichment, immune cell analysis (CIBERSORT), miRNA and transcription factor (TF) prediction, and drug-gene interaction analysis.
Main Results:
- Six key biomarkers (IL1B, TLR2, FCGR2A, SYK, FCER1G, HCK) were identified for CAD.
- A diagnostic model using these biomarkers showed high accuracy (AUC > 0.7).
- Differential expression of 10 immune cell types and regulatory relationships involving has-miR-1207-5p, RUNX1, and SPI were identified. Aspirin was among predicted drugs.
Conclusions:
- Six biomarkers associated with CAD phagocytic regulatory factors were identified.
- Expression regulatory networks provide insights into CAD pathogenesis.
- These findings support improved CAD diagnosis and potential treatment strategies.
Background:
Coronary artery disease (CAD) is the leading cause of death worldwide, and aberrant phagocytosis may be involved in its development. Understanding this aspect may provide new avenues for prompt CAD diagnosis.
Methods:
CAD-related information was obtained from Gene Expression Omnibus datasets GSE66360, GSE113079, and GSE59421. We identified 995 upregulated and 1086 downregulated differentially expressed genes (DEGs) in GSE66360. Weighted gene co-expression network analysis revealed a module of 503 genes relevant to CAD. Using clusterProfiler, we revealed 32 CAD-related PRFs. Eight candidate genes were identified in a protein-protein interaction network. Machine learning algorithms identified CAD biomarkers that underwent gene set enrichment analysis, immune cell analysis with CIBERSORT, microRNA (miRNA) prediction using the miRWalk database, transcription factor (TF) level predication through ChEA3, and drug prediction with DGIdb. Cytoscape visualized the miRNA -mRNA- TF, miRNA-single nucleotide polymorphism-mRNA, and biomarker-drug networks.
Results:
IL1B, TLR2, FCGR2A, SYK, FCER1G, and HCK were identified as CAD biomarkers. The area under the curve of a diagnostic model based on the six biomarkers was > 0.7 for the GSE66360 and GSE113079 datasets. Gene set enrichment analysis revealed differences in their biological pathways. CIBERSORT revealed that 10 immune cell types were differentially expressed between the CAD and control groups. The TF-mRNA-miRNA network showed that has-miR-1207-5p regulates HCK and FCER1G expression and that RUNX1 and SPI may be important TFs. Ninety-five drugs were predicted, including aspirin, which influenced ILIB and FCERIG.
Conclusion:
In this study, six biomarkers (IL1B, TLR2, FCGR2A, SYK, FCER1G, and HCK) related to CAD phagocytic regulatory factors were identified, and their expression regulatory relationships in CAD were further studied, providing a deeper understanding of the pathogenesis, diagnosis, and potential treatment strategies of CAD.
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