Skip to main content
. Author manuscript; available in PMC: 2020 Jul 1.
Published in final edited form as: Stem Cells. 2019 May 14;37(7):910–923. doi: 10.1002/stem.3021

Figure 5. Epigenetic and functional cardiac priming of CPCs by pIC.

Figure 5.

a) Expression of type I and type II HDACs in pIC primed vs. untreated CPCs from three hPSC lines measured by RT-qPCR, n = 3–4. JAG1 was upregulated and type II HDACs downregulated in all three lines, confirming consistency of day 5 priming.

b) chIP-qPCR of cardiac myofilament genes, JAG1, and chromosome 8 intergenic negative control as raw percent input binding to activating marks H3K9ac and H3K4me3, repressive mark H3K27me3, or rabbit IgG negative control, in hiPSC line 19-9-11, n = 4.

c) RT-qPCR of myofilament genes for day 9, 11, and 30 cardiomyocytes, fold change +/− pIC treated CPCs and day of onset of contractions and in hiPSC line 19-9-11, n=3.

d) Cardiac actin (AC1–20.4.2) immunostaining of NSGW mouse kidney xenografts day 30-post transplantation of primed and untreated CPCs from hiPSC line 19-9-11, n=3–4. ANOVA P < .05.

e) Sarcomeric myosin heavy chain (MF20) immunostaining of areas in (d) showing overlap with anti-human mitochondria (113–1) in confocal microscopy.

t test or post-hoc Holm P * < .05, ** < .01, *** < .001