Fig. 2: Hypertrophy versus hyperplasia in iPSC-derived CMs.

a Illustration of mitotic cells stained with the mitotic marker phospho-Ser10-histone 3 (p-H3) in iPSCs and dissociated CBs at d40. As a positive control, proliferative human iPSCs were treated for 12 h with 100 nM nocodazole (NC) to be arrested in mitosis. CMs show no proliferative behavior as compared to iPSCs, which were arrested in mitosis by NC treatment. b Cell cycle analysis of iPSC untreated and treated with NC as well as CMs treated with 100 µM l-phenylephrine (PE). Cell cycle analysis indicates that NC-treated iPSCs are mainly captured in the G2/M phase and stained positive for p-H3. Where PE-treated CMs are arrested in G1. c Dissociated CMs at d40 were treated with PE for 7 days. Both treated and untreated CMs remain p‑H3 negative. d The cell surface area of the stained CMs with the cardiac marker of cTNT (−PE and +PE) were quantified with Image J software, which indicates the increased cell size in response to PE’s pro‑hypertrophic activity. *P < 0.05, unpaired 2-tail t-test. n = 2, biological replicates. CM cardiomyocytes, cTNT cardiac troponin T, iPSC induced pluripotent stem cells, PE phenylephrine, p-H3 phospho-histone 3, NC Nocodazole.