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Fig. 3 | BMC Cardiovascular Disorders

Fig. 3

From: HiPSC-derived cardiomyocyte to model Brugada syndrome: both asymptomatic and symptomatic mutation carriers reveal increased arrhythmogenicity

Fig. 3

Sodium current (INa) densities and gating properties of hiPSC-CMs. (A-C) Typical examples of whole-cell INa traces recorded at room temperature from WT, asymptomatic and symptomatic CMs. (D) Current-voltage relationships of average INa densities. (E) Average voltage dependence of activation. (F) Voltage-dependence of steady-state inactivation curve. Peak sodium currents were normalized to maximum values and plotted as function of voltage. (G) Average fast (τfast) and slow (τslow) time constants of INa inactivation plotted as a function of membrane potential. (WT vs. asympt and WT vs. sympt, *P < 0.05). (H) Time-course of recovery after inactivation. Peak INa elicited by P2 were normalized (P2/P1) and plotted as function of the recovery interval. (I) The time-course of entry into the slow inactivation state. Peak INa elicited by P2 were normalized (P2/P1) and plotted as function of the duration of P1. Insets: Voltage-clamp protocol used in each experiment. Numbers in parenthesis represent the number of cells used. Data are presented as mean ± S.E.M.

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