Fig. 2: Increased ECM stiffness contributes to the progression of HCM pathophysiology. | Communications Biology

Fig. 2: Increased ECM stiffness contributes to the progression of HCM pathophysiology.

From: A maladaptive feedback mechanism between the extracellular matrix and cytoskeleton contributes to hypertrophic cardiomyopathy pathophysiology

Fig. 2

Representative ratiometric flavoprotein (a, b) and JC-1 (e, f) fluorescence recorded from wt cardiac myocytes plated on soft and stiff hydrogels before and after exposure to 10 μM BayK(+), or 10 μM BayK(−) in the absence or presence of nisoldipine (15 μM, Nisol). JC-1 studies were performed under calcium-free conditions (0 mM calcium). Arrows indicate addition of drugs. To confirm signals were mitochondrial in origin, FCCP (50 μM) was applied at the end of each flavoprotein experiment to increase flavoprotein oxidation. NaCN (40 mM) was applied at the end of each JC-1 experiment to collapse Ψm. Overall flavoprotein (c) and JC-1 (d) fluorescence for all myocytes (n) exposed to drugs as indicated, including mean ± SEM. d–h, flavoprotein (d) and JC-1 (h) fluorescence for cardiac myocytes (n, in suspension) isolated from cardiomyopathic cTnI-G203S mice and wt counterparts after exposure to BayK(+) or 10 μM BayK(−)17. All statistical significance determined by Kruskal-Wallis tests, or Browne-Forsythe and Welch ANOVA test (i).

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