Fig. 7From: Structural and electrophysiological dysfunctions due to increased endoplasmic reticulum stress in a long-term pacing model using human induced pluripotent stem cell-derived ventricular cardiomyocytesInhibition of calpain activity attenuated the adverse effects of pacing. Flow cytometry analysis of cardiac troponin T (cTnT) and MLC2v (a) demonstrated that the pharmaceutical inhibition of calpain activation significantly increased the cTnT+ and MLC2v+ cells ratio compared with that in the paced VCMs (b). Patch-clamp studies revealed that ICa, L density was significantly increased after the calpeptin treatment (c). In the calpeptin (5 μM)-treated group, the protein levels of cTnT (d) and L-type calcium channel (g) were increased by western blot analysis. The expression of apoptosis proteins (caspase-3, e; Bax/Bcl-2, f) that are involved in ER stress decreased markedly upon the calpeptin treatment compared with 100% Pace group. * p < 0.05, ** p < 0.005, *** p < 0.001 according to a one-way ANOVA testBack to article page