Cardiac hypertrophy-associated repression of H19 is
conserved among mice, humans, and pigs. (A) Abundance
of H19 in various mouse organs
(n = 3).
(B) Distribution of H19 in a
cardiac fraction of murine hearts (CM, cardiomyocytes; CF, cardiac
fibroblasts; EC, endothelial cells;
n = 8).
(C) H19 in stages of murine heart
development
(n = 4–5).
(D) H19 expression levels, heart
weight-to-tibia-length ratio (HW/TL), and ejection fraction (EF) over
the time course of heart failure progression (TAC, transverse aortic
constriction;
n = 5–8).
(E) H19 gene expression in human
induced pluripotent stem cell (iPSC)-derived cardiomyocytes after
pro-hypertrophic stimulation (Iso, isoproterenol;
n = 3).
(F) Contractile force measurements and human
H19 levels in human engineered heart tissue with
and without afterload enhancement (AE;
n = 6–8).
(G) Expression of human H19 in
patient-derived cardiac material compared to corresponding control
tissues (indicated as dashed line) (HOCM, hypertrophic obstructive
cardiomyopathy; LVAD, left ventricular assist device).
(H) H19 Expression in different
heart segments of hypertrophic pigs and Sham animals. Data are means
± SD. P-values were determined by two-tailed
unpaired Student’s t-test.
*P < 0.05;
**P < 0.01;
***P < 0.001.