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. 2015 Jan 23;5:7983. doi: 10.1038/srep07983

Figure 5. SHH signal pathway inhibits excitation-contraction coupling of ventricular cardiomyocytes.

Figure 5

(A) Representative time course of sarcomere length of control (dash line), N-SHH-treated (continuous line) and MPsSHH+-treated cardiomyocytes (dot line) for 4 h. (B) Resting sarcomere length in control, N-SHH-treated and MPsSHH+-treated cardiomyocytes. (C) Cell shortening (% of diastolic sarcomere length). (D) Representative time-course of Ca2+ transient (450/480 nm indo-1 fluorescence) of control (dashed line) cardiomyocytes and cardiomyocytes incubated with a recombinant SHH (N-SHH, continuous line) or MPsSHH+ (dotted line) for 4 h. (E) Diastolic Ca2+ levels in control, N-SHH-treated and MPsSHH+-treated cardiomyocytes. (F) Ca2+ transient amplitude. All parameters were measured in control (n = 253), N-SHH-treated (n = 82) or MPsSHH+-treated (n = 218) cardiomyocytes after incubation with phosphoinositide-3 kinase inhibitor, LY294002 (LY, 25 μM, n = 19), NOS inhibitor, Nω-nitro-L-arginine (L-NNA, 100 μM, n = 19) and SHH pathway inhibitor, cyclopamine (Ccl, 30 μM, n = 17 with N-SHH and n = 75 with MPsSHH+). Incubation with MPs lacking the SHH protein (MPsSHH-, n = 25) did not modify the shortening or Ca2+ transient. Data are mean ± SEM, *, p < 0.05 compared to control.