Fig. 2: RNAseq analysis at disease onset in D2-mdx and age-matched B10-mdx hearts. | Cell Death & Disease

Fig. 2: RNAseq analysis at disease onset in D2-mdx and age-matched B10-mdx hearts.

From: Failure to resolve inflammation contributes to juvenile onset cardiac damage in a mouse model of Duchenne muscular dystrophy

Fig. 2

Juvenile D2-mdx and B10-mdx hearts at disease onset (6 wk ± 0.5 wk) were analyzed by bulk tissue RNAseq. A Dimensionality reduction of whole transcriptomic data via PCA (n = 3−4 hearts/genotype) to assess sample clustering and inter-/intra-sample variance. B Differential gene expression analysis depicted via heatmap plot of 2719 DEGs observed between D2-mdx (blue) and B10-mdx (red), with 1586 genes upregulated for D2-mdx and 1133 genes upregulated for B10-mdx. Expression is z-score values of variance-stabilizing transformation (VST) normalized data. C Gene Ontology (GO) analysis performed using Cytoscape and EnrichmentMap plugins to identify networks of related GO terms groups found upregulated (red dots) in juvenile D2-mdx hearts relative to B10-mdx. Pink clusters refer to inflammatory-related GO terms, while blue clusters refer to extracellular matrix-related GO terms. D, E Boxplots showing VST normalized gene expression levels for top 20 differentially expressed inflammation-related (D; GOBP:Inflammatory Response) and extracellular matrix-related (E; GOBP:External Encapsulating Structure) transcripts observed between juvenile D2-mdx and B10-mdx hearts. Refer to Supplementary Fig. 3 for additional details.

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