Fig. 7. Pharmacologic response of CM-AI cryopreserved hiPSC-CMs to PDE4 inhibition in 96-well high-throughput electrophysiology screen.
a Cryopreserved TTN-GFP atrial hiPSC-CMs phase contrast and GFP images, 20×. b Zoomed image of sarcomere structures in hiPSC-CMs. c Representative time-space plots indicate functional monolayer electrophysiological activations across the width of each well of the 96-well plate (9 mm diameter). Rolipram increased hiPSC-CM monolayer beat rate. d Representative calcium transient traces indicating the effect of rolipram to increase calcium transient amplitude. e Rolipram increased 2D monolayer beat rate (VEH = 80.0 ± 11.8; 1.0 µM Rolipram = 113.3 ± 33.0; 10.0 µM Rolipram = 129.2 ± 9.4 bpm, n = 8 per group). One way ANOVA, multiple comparisons, *P = 0.01; ***P = 0.0004. f Rolipram increased calcium transient amplitude (VEH = 0.53 ± 0.17; 1.0 µM Rolipram = 0.72 ± 0.40; 10.0 µM Rolipram=1.22 ± 0.50 ∆F/F0, n = 8 per group). One way ANOVA, multiple comparisons, **P = 0.004. g Rolipram increased calcium impulse conduction velocity (VEH = 23.5 ± 4.1; 1.0 µM Rolipram = 30.3 ± 17.6; 10.0 µM Rolipram = 47.9 ± 20.4 cm/s, n = 8 per group). One way ANOVA, Brown-Forsythe and Welch tests, multiple comparisons, *P = 0.02.
