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. 2021 Oct 19;10:e65512. doi: 10.7554/eLife.65512

Figure 2. cahErbb2 induces NRVM cycle entry in monolayers and promotes sarcomere disassembly in NRVMs and hiPSC-CMs.

(A) Schematic of experimental design in NRVM monolayers. (B–E) Flow cytometry analysis of mCherry+ NRVMs showing (B) fold-change (FC) in EdU incorporation relative to control LV-treated NRVMs, (C) percentage of H3P+ CMs, and (D, E) percentage of 2N and >2N cells in all CMs (D) and EdU+ CMs (E). (F) Representative immunostaining images of sarcomeric α-actinin showing sarcomeric structure in LV transduced NRVMs and hiPSC-CMs. (G) Relative expression of Erbb2, sarcomeric genes (Myh6, Myh7, and Tnnt2), and dedifferentiation marker Runx1 in cahErbb2-transduced versus control hiPSC-CMs. Data: box and whiskers showing distribution and min to max. Column graphs showing mean+ SD (*p<0.05, **p<0.01, ***p<0.001 vs. Ctrl LV). hiPSC-CM, human-induced pluripotent stem cell-derived cardiomyocyte; LV, lentiviral vector; NRVM, neonatal rat ventricular myocyte.

Figure 2.

Figure 2—figure supplement 1. cahErbb2 expression does not affect non-CM abundance or CM size in hiPSC-CM and NRVM monolayers.

Figure 2—figure supplement 1.

(A) Quantification of non-CM abundance based on cTnT staining and flow cytometry analysis of hiPSC-CMs (left) and Mef2c expression in immunostained NRVMs (right). (B) Relative CM size in hiPSC-CMs (left) and NRVMs (right) quantified from flow cytometry forward scatters. Data: box and whiskers showing distribution and min to max (*p<0.05, **p<0.01, ***p<0.001 vs. Ctrl LV). hiPSC-CM, human-induced pluripotent stem cell-derived cardiomyocyte; LV, lentiviral vector; NRVM, neonatal rat ventricular myocyte.