Fig. 1: Identification of cardiomyocyte-derived USP13 as a vital factor in cardiac hypertrophy. | Nature Communications

Fig. 1: Identification of cardiomyocyte-derived USP13 as a vital factor in cardiac hypertrophy.

From: Cardiomyocyte-derived USP13 protects hearts from hypertrophy via deubiquitinating and stabilizing STAT1 in male mice

Fig. 1

a The mRNA profile of DUBs in Ang II-induced mouse hypertrophic myocardium was showed from a published transcriptome data (n = 3; GSE221396; P values were determined by Wald test from DESeq2 software with Benjamini-Hochberg’s correction). b RT-qPCR analysis of Usp13 mRNA level in Ang II- and TAC- induced mouse hypertrophic myocardium (n = 6) as well as human hypertrophic myocardium (n = 4; NCH non-cardiac hypertrophy, CH cardiac hypertrophy) (P values were determined by two-tailed unpaired t test). c Representative western blot of USP13 in Ang II- and TAC- induced mouse heart tissues (upper) and corresponding quantitative analysis (below, n = 6, P values were determined by two-tailed unpaired t test). d–g A single-cell mRNA sequencing was performed in hearts from TAC-treated mice (For each group, single-cell suspensions from 3 to 4 hearts were pooled as 1 sample). d tSNE plot showing 5 main cell types, including cardiomyocytes (CM), fibroblasts (FB), macrophages (MP), endothelial cells (EC) and pericytes (PC). e Biaxial scatter plot showing the expression pattern of Usp13 in these cell types. f UMAP distribution of clustering revealed 3 functional cardiomyocyte clusters. g Dot plot indicated the relative expression of Usp13 in the different functional cardiomyocyte clusters. h The cellular origin of USP13 in Ang II- (left) and TAC- (right) induced heart sections was revealed by immunofluorescence staining (Red: USP13; Green: α-actinin). For b-c, data are presented as mean ± s.e.m.

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