Figure 1

MMP-9 deficiency prevents ventricular arrhythmia.

(A) MMP-9 enzymatic activity in the ventricular tissue after Ang II treatment in WT mice was assessed by zymography (n = 4, *P < 0.05). (B) Representative image of MMP-9 ventricular activity by zymography. Cropped blots are displayed, and full-length blots are included in Supplementary Fig. S10. (C) MMP-9 protein expression in the isolated ventricular cardiomyocytes as determined by Western blot analysis (n = 4, *P < 0.05). (D) Colocalization of MMP-9 and myofibrils. (E to H) The incidence (E) and duration (F) of ventricular arrhythmia episodes after the burst ventricular stimulation and ventricular arrhythmia induction threshold (G) were partially reduced in the MMP-9^+/− mice and completely prevented in the MMP-9^−/− mice (n = 10 for each group, ^#P < 0.05 vs. WT + Ang II). (H) Representative ECG and intracardiac tracing after the burst ventricular stimulation. Polymorphic ventricular tachycardia was induced in the WT mice after Ang II treatment. However, ventricular arrhythmia was not inducible in the MMP-9^−/− mice after Ang II treatment. Data are shown as the mean ± SEM.