Figure 3. Genetic deletion of ENPP1 leads to enhanced cardiac repair and better preservation of postinjury heart function.

(A) Western blotting for ENPP1 expression in the hearts of ENPP1CKO animals at 7 days following cardiac injury and (B) quantitative densitometry of ENPP1 expression (n = 4). (C) B mode and M mode echocardiogram demonstrating better contractile function with decreased chamber dilatation at 4 weeks following cardiac injury (green arrows, diastole; yellow arrows, systole). (D) EF and fractional shortening as well as LV chamber size (LVID) in systole and diastole over 4 weeks after cardiac injury in control and ENPP1CKO animals. (E) Pie chart demonstrating fraction of animals with mild, moderate, and severe reductions in EF. (F) Masson trichrome staining demonstrating scar size (blue) measured at the apex and midventricle and (G) quantitation of differences in scar size as a fraction of the LV surface area. (H) Pie chart showing animals (%) with mild, moderate, and severe fibrosis. (I) Heart weight (HW), body weight (BW), and HW/BW ratios measured at 4 weeks following cardiac injury and (J) cardiac troponin T immunostaining to determine myocyte surface area (arrowheads) at the border zone and quantitation of myocyte surface area. Scale bar: 10 μm. (K) Number of capillaries (CD31 staining, arrowheads) in ENPP1CKO and control animals at 4 weeks after heart injury and quantitation of capillary density. Scale bar: 10 μm. Data are represented as mean ± SEM. **P < 0.01; *P < 0.05, ordinary 1-way ANOVA with Tukey’s multiple comparison test (B), ordinary 2-way ANOVA with Šidák’s multiple comparisons test (D), or 2-tailed Student’s t test (G, I–K). n = 14 in control and n = 16 in ENPP1CKO animals (D, E, and G– K).