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. Author manuscript; available in PMC: 2021 May 19.
Published in final edited form as: Sci Transl Med. 2019 Oct 9;11(513):eaaw6419. doi: 10.1126/scitranslmed.aaw6419

Figure 5. β-adrenergic signaling regulates cytokinesis in cardiomyocytes from ToF/PS patients.

Figure 5.

(A) Cardiomyocytes from ToF/PS patients exhibit decreased levels of Ect2 mRNA. Each symbol represents one cycling cardiomyocyte. (B) The percentage of Ect2-positive cycling cardiomyocytes was reduced in ToF/PS patients, compared with fetal human hearts. (A-B, Fetal: n = 71 cardiomyocytes from 4 hearts, ToF/PS: n = 13 cardiomyocytes from 3 hearts). (C, D) β-AR signaling regulates cytokinesis failure in cultured human fetal cardiomyocytes (n = isolations from 3 hearts; Ctrl: control; Fsk: Forskolin, Prop: Propranolol; Dobu: Dobutamine: 10 μM), measured by reduced formation of binucleated daughter cells (C) and higher prevalence of Ect2-positive midbodies (D). (E) Propranolol increases completion of cytokinesis in cultured ToF/PS cardiomyocytes (n = cultures from 3 patients). (F) Cellular model connecting cytokinesis failure to endowment changes. (G) Molecular model of cytokinesis failure in cardiomyocytes. Scale bar: 40 μm (C). Statistical significance was tested with T-test (A) and one-way ANOVA with Bonferroni’s multiple comparisons test (C-E).