Integrated microarray analysis to identify potential biomarkers and therapeutic targets in dilated cardiomyopathy

Figures

• 

  Figure 1.. Identification of DEGs between patients with DCM and healthy controls. (A) Workflow identifying DEGs between patients with DCM and healthy controls. (B) Venn diagram of the DEGs outputted by metaMA and RankProd. A total of 1,943 DEGs were outputted by metaMA, while 1,390 DEGs were outputted by RankProd, among which 898 DEGs were overlapping. (C) Components of the DEGs. Among the 898 DEGs, 424 DEGs were upregulated and 474 DEGs were downregulated. DEGs, differentially expressed genes; DCM, dilated cardiomyopathy.

• 

  Figure 2.. Validation of DEGs. (A) Clustering heat map of DEGs in GSE79962. (B) Clustering heat map of DEGs in GSE3585. The ordinate is the gene name, and the abscissa is the sample name. Red indicates high expression, while blue indicates low expression. Group DCM represents samples from patients with DCM, and NC represents samples from healthy controls. DEGs, differentially expressed genes; DCM, dilated cardiomyopathy; NC, healthy control.

• 

  Figure 3.. Functional annotation of DEGs. GO analysis of the (A) upregulated DEGs and (B) downregulated DEGs. The ordinate is the GO term name, and the abscissa is the count of DEGs enriched in the GO term. P-value of the enriched term is reflected by the color of the bar. KEGG pathway enrichment of the (C) upregulated DEGs and (D) downregulated DEGs. The ordinate is the name of the KEGG pathway, and the abscissa is the fold enrichment of the pathway. The count of DEGs is represented by bubble size and P-value by color. DEGs, differentially expressed genes; GO, Gene Ontology; KEGG, Kyoto Encyclopedia of Genes and Genomes; TGF-β, transforming growth factor β; ECM, extracellular matrix; PKG, protein kinase G.

• 

  Figure 4.. Construction of the PPI network. PPI network of DEGs. Red nodes are upregulated DEGs, while blue nodes are downregulated DEGs. Edges between nodes represent interactions of DEGs. DEGs, differentially expressed genes; PPI, protein-protein interaction.

• 

  Figure 5.. Identification of important modules and hub genes in the PPI network. (A) The first module, (B) the second module and (C) the third module of the PPI network detected by the MCODE plug-in and ranked from largest to smallest by score. Red nodes are upregulated DEGs, while blue nodes are downregulated DEGs. Edges between nodes represent interactions of DEGs. (D) GO analysis of the DEGs in module 1, module 2 and module 3. The orange bar represents the count of DEGs enriched in the GO term, and the purple dot represents the -log10P-value. (E) Venn diagram of the top 20 genes calculated by four algorithms. DEGs, differentially expressed genes; PPI, protein-protein interaction; GO, Gene Ontology; BMP, bone morphogenetic protein; MNC, Maximum Neighborhood Component; DMNC, Density of Maximum Neighborhood Component; MCC, Maximal Clique Centrality.

• 

  Figure 6.. Validation of the hub genes in the mouse DCM model. (A) Representative echocardiography images of mice treated with saline and DOX. (B) Ejection fraction, (C) fractional shortening, (D) LVIDs, (E) LVIDd, (F) LVPWd and (G) IVSd of mice treated with saline or DOX. (H) Relative expression of PENK, CHRDL1, CALU, IGFBP3 and CP in the hearts of mice treated with DOX, normalized to the expression of β-actin. n=6. *P<0.05, **P<0.01 vs. saline. DOX, doxorubicin; LVIDs/d, left ventricular internal diameter end systole/diastole; LVPWd, left ventricular posterior wall end diastole; IVSd, interventricular septal end diastole; PENK, proenkephalin; CHRDL1, chordin like 1; CALU, calumenin; IGFBP3, insulin-like growth factor binding protein 3; CP, ceruloplasmin.