Supplementary Figure 3: Angiotensin II induced stress induces premature heart failure in young G2 mice.
From: Role of telomere dysfunction in cardiac failure in Duchenne muscular dystrophy

(a) Scheme of experimental procedure. Mice were tested for cardiac function by echocardiography prior to minipump insertion. Osmotic minipumps delivering either saline (S) or Angiotensin II (A) were implanted subcutaneously into 12-week-old asymptomatic G2 and control mice and cardiac function was measured weekly. (b) Representative images 3 weeks after minipump insertion show left ventricular dilation and compromised contractility only in G2 hearts that received Angiotensin II (See also Supplementary Videos S2.). (c) Echocardiographic measurements over time show reduction in fractional shortening (FS), increase in left ventricular transverse area in diastole (LVTAd) and increase in left ventricular transverse area in systole (LVTAs), only in hearts of G2 animals with Angiotensin II, compared to the control mice. Data are represented as mean±SEM (n = 5–6); ANOVA followed by Bonferonni test for multiple comparisons, ** indicates P<0.01 and ***P<0.001. (d) Representative histological analysis using Trichrome staining on longitudinal paraffin sections show increased fibrotic tissue deposition in hearts of Angiotensin II treated G2 mice compared to controls. (e) Quantification of fibrosis. Data are represented as mean±SEM (n = 4); Two-tailed, unpaired Student’s t-test, P value is indicated. Source data are shown in Supplementary Table S1.