Fig. 1: PTRH2 mRNA and protein is downregulated in PPCM female patient hearts.

a–c PTRH2, ACTA1, and MYH7 mRNA quantitation from female normal donor and PPCM LV samples. Data shown is from biologically independent human samples/group. PTRH2 (n = 4; p = 0.001), ACTA1 (n = 5; p = 0.00073), and MYH7 (n = 5; p = 0.0198). d, e Immunoblot (left) and protein quantification (right) of PTRH2 (n = 5; p < 0.0001) and cardiomyopathy markers ACTA1(n = 5; p < 0.0001) and β-MHC (n = 5; p = 0.003) in normal donor and PPCM LV samples. Data shown is from biologically independent human LV samples/group. Statistical test (a–e) was by Two-tailed unpaired t-test. Error bars are mean + s.e.m. Each dot on graph represents an independent biological LV sample from either normal donor or PPCM. f Normal donor or PPCM LV sections immunostained for PTRH2. Scale bar, 50 μm. g Experimental workflow for RNA-seq on normal donor and PPCM LV heart samples. h Differential gene expression (DEG) from RNA-seq analysis of PPCM compared to normal donor LV heart samples. i Heat map of 50 DEGs (row normalized) in PPCM versus normal donor LV samples; increased (red), decreased (green), baseline value (black). j STRING network map of up- and down-regulated genes identified in PPCM/DCM, Cardiac Hypertrophy, PI3K/AKT and Integrin signaling pathways in PPCM LVs compared to normal donor LVs. Source data are provided as a Source Data file. Schematic in g was created using BioRender (https://biorender.com). See Supplementary Fig. 1.