Figure 2
Hearts from adult mice with global 11β-HSD1 deficiency are hypomorphic and have shorter cardiomyocytes. Ultrasound analysis
(A) reveals a significant reduction in left ventricular dimensions in 12-week-old Hsd11b1−/− (open bars) compared with control wild-type mice (filled bars). Reduction in heart size was confirmed when post-mortem heart
weight was compared with body weight (B). LV dimensions (left ventricular end-diastolic area, solid red (Hsd11b1−/−) and black (control wild type), and left ventricular end-systolic area, hatched red (Hsd11b1−/−) and black (control wild type)) were not influenced by the loss of 11β-HSD1 from late gestation until 6 weeks of age (C).
In adult hearts, there was no effect of 11β-HSD1 deficiency (red) on the distribution of cardiomyocyte cross-sectional area
(D), but the length of individual cardiomyocytes (E) isolated from Hsd11b1−/− hearts was significantly less than that isolated from control wild-type hearts (black).*P < 0.05, ***P < 0.005, n = 5–8.