Fig. 5: Differential EV-signaling in cardiomyocyte populations upon hypertrophic remodeling. | Communications Biology

Fig. 5: Differential EV-signaling in cardiomyocyte populations upon hypertrophic remodeling.

From: Single-cell transcriptomics reveal extracellular vesicles secretion with a cardiomyocyte proteostasis signature during pathological remodeling

Fig. 5

a UMAP plot of unbiased reclustering of the cardiomyocyte cluster identified after scRNA-seq and data integration. Cells were isolated from control (sham) and hypertrophic (transaortic constriction (TAC)) hearts at an early compensatory (CH) and late failing (FH) stages (average of 650 cells per condition and stage). Four sub-clusters were identified (CM1-CM4). Corresponding hypertrophic stress scores as defined by the expression of Acta1, Nppa, Nppb and Ankrd1 are depicted for all cells. b Representative dot plots showing expression levels for the stress genes Myh7, Nppa, cardiac Wnt-target genes Dstn, Rock2, Bambi, Ccnd2 and Wnt inhibitors Kremmen1, Shisa4, Apc in clusters CM1-CM4 from sham and TAC hearts of CH (left) and FH (right) stages. Violin plots showing Wnt signaling target and stress scores in the different CM clusters for CH (c) and FH (d) stages. e Selected top categories from GO biological processes enrichment of overlapping DEGs obtained from sham vs TAC comparison in CH (left) and FH (right). GO enrichment represents –log10 p-value (p-value <0.05) and term fusion was applied.

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