Oxidative Medicine and Cellular Longevity / 2015 / Article / Fig 1

Research Article

Oxidative Stress in Dilated Cardiomyopathy Caused by MYBPC3 Mutation

Figure 1

DCM hearts display contractile dysfunction, fibrosis, and myocardial disarray. (a) Representative parasternal long-axis M-mode echocardiographic images of WT and DCM hearts. Left ventricular internal diameter (LVID) is depicted by white lines (note: difference in scale between images). LVID at (b) peak diastole and (c) peak systole in WT and DCM hearts ( hearts, ). Functional measurements derived from LVID measurements showing (d) ejection fraction (EF) and (e) fractional shortening (FS) in WT and DCM hearts ( hearts, ). (f) H&E labeled whole hearts from WT and DCM animals. (g) H&E or (h) Masson’s trichrome-labeled regions of interest (ROI) from WT and DCM hearts. (i) Quantification of cellularity based on nuclear area between WT ( hearts, 5 sections per heart) and DCM hearts ( hearts, 5 sections per heart). (j) Quantification of fibrosis (trichrome staining) area between WT ( hearts, 20 sections per heart) and DCM hearts ( hearts, 20 sections per heart; ). Data are represented as mean ± SEM. Significant differences () between mean values were determined using Student’s -test.
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