Linagliptin decreases F
passsive by increasing titin phosphorylation at N2Bus S4010 in human cardiomyocytes in vitro. A, Cardiomyocyte passive stiffness in human cardiomyocytes treated with 300 ng/mL DPP‐4, 100 nmol/L linagliptin and 300 ng/mL DPP‐4, or control (DMSO/PBS) for 30 min (n = 3 different left ventricular tissues measuring at least 12 cardiomyocytes from each left ventricular tissue per condition). B, PKA‐mediated N2Bus S4010 phosphorylation and representative Coomassie Blue stained‐PVDF membranes and (C) PKG‐dependent N2Bus S4099 phosphorylation in human cardiomyocytes (n = 5 different left ventricular tissues) treated with vehicle control (DMSO/PBS), 300 ng/mL DPP‐4, 300 ng/mL DPP‐4 and 100 nmol/L linagliptin, or 100 nmol/L linagliptin for 2 h. F
passive, passive stiffness; N2Bus, N2B unique sequence. Panel A was analysed using a two‐tailed unpaired Student t test with *P < .05. Panel B and C were analysed using a one‐way ANOVA with Dunnett's multiple comparison post hoc test with *P < .05 and ***P < .001 comparing control, DPP‐4 + Lina and Lina to DPP‐4