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. 2015 Nov 30;112(50):E7003–E7012. doi: 10.1073/pnas.1513843112

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Fig. 5. — Myofilament Ca²⁺ sensitivity and sarcomere stiffness, in the presence of 100 µM ADP, in idiopathic dilated cardiomyopathy (IDCM) and hypertrophic cardiomyopathy (HCM) membrane-permeabilized cardiomyocytes. Normalized force–Ca²⁺ relationships before and after protein kinase A (PKA) in the presence of ADP for MYH7_mut (A) and MYBPC3_mut (B) heart samples. Myofilament Ca²⁺ sensitivity in the presence of ADP (EC₅₀) before (C) and after (D) PKA treatment in IDCM, HCM, and donor samples. Residual force, a measure of sarcomere stiffness, at high Ca²⁺ with 100 µM ADP (EC₅₀) before (E) and after (F) PKA treatment in IDCM, HCM, and donor samples. Data were compared using multilevel analysis. N, number of samples; n, number of cardiomyocytes. HCM_smn, sarcomere mutation-negative HCM samples (n = 3, n = 8); IDCM (n = 4, n = 18); MYBPC3_mut, myosin-binding protein-C (missense) mutations (n = 3, n = 10); MYBPC3_trunc, myosin-binding protein-C (truncating) mutations (n = 4, n = 12); MYH7_mut, myosin heavy-chain mutations (n = 3, n = 10); TNNI3_mut, cardiac troponin I mutation (n = 1, n = 4); TNNT2_mut, cardiac troponin T mutation (n = 1, n = 4). Fourteen cardiomyocytes from five nonfailing hearts (donor) served as controls.