Figure 2: Bmi1 activation blocks development of cardiac hypertrophy.
From: Bmi1 limits dilated cardiomyopathy and heart failure by inhibiting cardiac senescence
(a) Gross cardiac phenotype of Bmi1fl;αMHCCre mice and Bmi1fl controls. Representative views are shown of external anatomy and H&E staining on sections in adult hearts (12-week-old; top two rows; bars, 50 mm), Masson’s trichrome staining to detect fibrosis (third row; bars, 40 μm) and left ventricular muscle sections stained with WGA to detect cardiomyocyte borders (bottom row; bars, 10 μm). (b) M-mode echocardiographic analysis of Bmi1fl;αMHCCre and Bmi1fl mice. IVSd, diastolic interventricular septal wall thickness; LVDd, diastolic left ventricular internal dimension; LVDs, systolic left ventricular internal dimension; LVPWd, diastolic left ventricular posterior wall thickness; FS, fractional shortening of left ventricle dimension; EF, ejection fraction; LVmass, left ventricular mass. Data are means±s.d. (n=13, **P<0.001, *P<0.05; Student’s t-test). (c) Thoracic MRI of Bmi1fl;αMHCCre and Bmi1fl mice in transverse view, showing both heart and lungs (top), and in coronal view (bottom). Scale bars, 2.5 mm. (d) Representative Perls iron staining of lung sections from representative 12-week-old Bmi1fl;αMHCCre and Bmi1fl littermates (bars, 30 μm). (e) Lung weight in 12-week-old Bmi1f/f;αMHCTM-Cretg/+ and Bmi1+/+;αMHCTM-Cretg/+ mice (means±s.d.; n=10, *P<0.05; Student’s t-test). (f) Kaplan–Meier survival curve for Bmi1fl;αMHCCre mice and Bmi1fl littermates (means±s.d.**P<0.001; Student’s t-test).
