Skip to main content
. Author manuscript; available in PMC: 2021 Aug 28.
Published in final edited form as: Circ Res. 2020 Jul 1;127(6):827–846. doi: 10.1161/CIRCRESAHA.119.315999

Figure 1. EPRS is upregulated in human and mouse heart failure.

Figure 1.

(A) Glutamyl-prolyl-tRNA synthetase (EPRS) is a common hit of upregulated ARSs and ARSs with a genetic association in human and mouse heart disease, but not induced in human physiologic muscle hypertrophy.

(B) EPRS mRNA is increased in failing human hearts (n=17) compared to non-failing donor hearts (n=6). 18S rRNA is used as a loading control.

(C) EPRS protein is increased in failing human hearts compared to non-failing donor hearts. Representative Western blot results are shown.

(D) Quantification of Western blot results from all human heart samples indicates elevated expression of EPRS in failing human hearts (n=17) compared to non-failing donor hearts (n=8). GAPDH is used as a loading control for quantification.

(E-F) EPRS mRNA and protein expression are increased in the hearts from a 4-week ISO infusion induced mouse HF model compared to vehicle infused hearts while Iars (Isoleucyl-tRNA synthetase) mRNA remains unchanged. 18S rRNA and GAPDH are used as loading controls for mRNA and protein quantification, respectively.

(G-H) EPRS mRNA and protein expression are increased in the hearts from an 8-week TAC surgery-induced mouse HF model. Gars (glycyl-tRNA synthetase) is a negative control ARS in the TAC model. 18S rRNA and GAPDH are used as loading controls for mRNA and protein quantification, respectively.

Comparisons were performed by non-parametric unpaired Mann-Whitney test for B, D, E, G.