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. Author manuscript; available in PMC: 2012 Sep 1.
Published in final edited form as: Nat Genet. 2012 Jan 22;44(3):343–347. doi: 10.1038/ng.1068

Figure 1.

Figure 1

Ezh2 limits cardiac growth and fibrosis. (a) Adult mice in which Ezh2 was deleted in second heart field progenitors (Ezh2fl/fl; Mef2cAHF::Cre) present hypertrophied right ventricle, with increased (b) heart weight to tibia length ratio (mg/mm), as compared to controls (Ezh2fl/fl). Ezh2fl/fl (blue bars) and Ezh2fl/fl; Mef2cAHF::Cre (red bars). (c) Wheat germ agglutinin (WGA) staining of heart sections in control (Ezh2fl/fl) or Ezh2-deficient (Ezh2fl/fl; Mef2cAHF::Cre) right ventricle (RV) and left ventricle (LV). (d) Cardiomyocyte cell surface area in Ezh2fl/fl (blue bars) or Ezh2fl/fl; Mef2cAHF::Cre (red bars) hearts. (e) Tissue disorganization and fibrosis, as revealed with Masson’s trichrome staining. In b and d, bars represent the mean +/− S.D. of measurements from at least three hearts per genotype. * indicates P < 0.05. (f) Vimentin staining of RV and LV of Ezh2fl/fl or Ezh2fl/fl; Mef2cAHF::Cre hearts. (g) Pecam staining showing invaginations of endocardium into myocardium (arrows). In f,g, the red arrow points to endocardial lining of the RV lumen. Reference bars in (a) and (e) (upper panel) = 0.5 cm; (e) (lower panel) = 100 µm; (c) = 25 µm; (f) and (g) = 100 µm.