Fig. 3: MLP-deficient hESC-CMs exhibit abnormal Ca2+ handling properties. | Cell Death & Disease

Fig. 3: MLP-deficient hESC-CMs exhibit abnormal Ca2+ handling properties.

From: MLP-deficient human pluripotent stem cell derived cardiomyocytes develop hypertrophic cardiomyopathy and heart failure phenotypes due to abnormal calcium handling

Fig. 3

a Schematic demonstrating the GCaMP-expression cassette that was integrated into AAVS1 of WT and MLP KO hESCs via nickase CRISPR/Cas9 editing. b Space-averaged calcium transients showing parameters measured for analysis of calcium handling. c Representative line-scan images in WT-GCaMP and MLP KO-GCaMP hESC-CMs at days 15, 22, and 30. d–f Quantification of peak, time to peak, and calcium transient duration in WT-GCaMP and MLP KO-GCaMP hESC-CMs (n = 15 cells per group). g Representative Ca2+ transients induced with 10 mM caffeine in Ca2+-free conditions between WT-GCaMP and MLP KO-GCaMP hESC-CMs at days 15, 22, and 30 (n = 5 cells per group). h–j Peak amplitude, transient duration, and decay time in caffeine-evoked Ca2+ transients WT-GCaMP and MLP KO-GCaMP hESC-CMs. Results are presented as means ± S.E.M. of three independent experiments. *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001; ns, not significant, unpaired two-sided Student’s t test

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