Pharmacological rescue of SLC25A6 overexpression and slc25a6 knockdown phenotypes. (A) Systolic duration normalized to heart period determined from high-speed video recordings of the heart ventricle. Systolic interval prolongation induced by slc25a6 knockdown (slc25a6 KD) is normalized by glybenclamide treatment (slc25a6 KD + glybenclamide). (B) Neither slc25a6 knockdown (slc25a6 KD) nor glybenclamide treatment (control KD + glybenclamide and slc25a6 KD + glybenclamide) affects heart rate. Data in (A,B) were compiled from four independent experiments, each encompassing all four groups. n(Control KD) = 28, n(Control KD + glybenclamide) = 37, n(slc25a6 KD) = 26, n(slc25a6 KD + glybenclamide) = 25. (C) Systolic interval normalized to heart period determined from high-speed video recordings of the heart ventricle. Systolic interval shortening induced by SLC25A6 overexpression (SLC25A6 mRNA) is diminished by pinacidil treatment (SLC25A6 mRNA + pinacidil). (D) Neither SLC25A6 overexpression (SLC25a6 mRNA) nor pinacidil treatment (Control mRNA + pinacidil and SLC25A6 mRNA + pinacidil) affects heart rate. Data in (C,D) were compiled from three independent experiments, each encompassing all four groups. n(Control mRNA) = 18, n(Control mRNA + pinacidil) = 16, n(SLC25A6 mRNA) = 15, n(SLC25A6 mRNA + pinacidil) = 17. Statistical analyses were performed by one-way ANOVA with Tukey´s post-test. *p < 0.05, **p < 0.01, ****p < 0.0001.
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