Fig. 4.

E2A deficiency significantly up-regulated the ratio of nodal-like CMs in hESC cardiac-specific differentiation.

(a) Whole-cell patch-clamp recording showed that nodal-like CMs increased to 41.3%, while ventricular-like CMs decreased to 39.1% after E2A knockout CMs derived from H7. (b) Low magnification bright field picture of the CMs monolayer seeded in MEA plates. (c) Representative snapshots of color map depicting electrical signal propagation of monolayer CMs. The color maps showed that the electrical signal is initiated at the bottom right corner (red) and is propagated to the upper left corner (blue) in wildtype CMs while E2A deficiency led to disruptive propagation of electrical signals with multiple initiation sites indicated by black arrows. (d) Electric pulse pattern of wildtype and E2A deficient CMs derived from H7 hESCs. (e) Quantification of FPD, ISI and cFPD (ratio of FPD/ISI) in wildtype and E2A knockout CMs. All data are presented as mean ± SEM. All data are presented as mean ± SEM, *** P value <0.001, # P value <0.0001(Two-tailed Student's t-test). (f) Expression of MLC-2v⁺ reduced, while TBX18⁺ increased after E2A knockout CMs derived from H7 hESCs. (g) Statistic of MLC-2v+ cells in wildtype and E2A knockout CMs derived from H7 hESCs. All data are presented as mean ± SEM, # P value <0.0001 (Two-tailed Student's t-test). (h) Statistic of TBX18+ cells in wildtype and E2A knockout CMs derived from H7 hESCs. All data are presented as mean ± SEM, # P value <0.0001 (Two-tailed Student's t-test).