Fig. 7.

Dysruption of [Ca²⁺]_i homeostasis in PKP2-cKO cardiomyocytes at 21 dpi. a Laser scanning confocal image of Ca²⁺ in control (top) and PKP2-cKO (bottom) permeabilized cardiomyocytes. b Sarcoplasmic reticulum (SR) Ca²⁺ leak in control (n = 30 cells from three hearts, black) and PKP2-cKO cardiomyocytes (n = 23 cells from three hearts, red). Statistical difference was estimated by measuring the average of spontaneous Ca²⁺ release without any stimulation. **p < 0.01 vs. control. c SR Ca²⁺ load estimated by measuring the peak of caffeine-induced Ca²⁺ release from control (n = 30 cells from three hearts, black) and PKP2-cKO permeabilized cardiomyocytes (n = 23 cells from three hearts, red) relative to the fluorescence intensity at baseline (F ₀). Given that cells were permeabilized, F ₀ was the same for control and for PKP2-cKO. *p < 0.05 vs. control. d Ratio between Ca²⁺ leak and SR Ca²⁺ load in permeabilized cells, **p < 0.01 vs. control. e Peak of caffeine-induced Ca²⁺ release (F) in control (n = 33 cells from three hearts, black) and PKP2-cKO intact cardiomyocytes (n = 34 cells from three hearts, red) relative to fluorescence at baseline (F _baseline). f Diastolic [Ca²⁺]_i in control (n = 10 cells from three hearts) and PKP2-cKO (n = 10 cells from three hearts) cardiomyocytes. Student’s t-test *p < 0.05. This result indicates that F at baseline (F _baseline) for the data in e was not the same for the two groups. The combined data in e and f indicate an increase in SR load in intact cells. g Representative confocal line-scan images of Ca²⁺ sparks recorded in control and PKP2-cKO cardiomyocytes. h, i Bar graphs depicting Ca²⁺ spark amplitude (F/F ₀) and Ca²⁺ spark frequency, respectively, measured as the number of events per unit time and length in control (n = 200 sparks, N = 27 cells from three hearts, black) and PKP2-cKO intact cardiomyocytes (n = 457 sparks, N = 30 cells from four hearts, red). Student’s t-test, ***p < 0.001 vs. control