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. 2006 Aug 1;103(32):11946–11951. doi: 10.1073/pnas.0510138103

Fig. 3.

Fig. 3.

Echocardiographic and postmortem analysis of mice at 2 wk after TAC reveals inhibition of concentric hypertrophy and smaller cross-sectional cell area in AKT-TAC relative to NTG-TAC hearts. (a) LV anterior wall thickness. (b) LV end-diastolic diameter. (c) LV fractional shortening. (d) heart weight/tibia length in NTG-sham (n = 8), NTG-TAC (n = 12), AKT-sham (n = 8), and AKT-TAC (n = 12) at 2 wk after surgery. (e) representative heart sections from sham or TAC of NTG or AKT mice. Cell membrane (green) and nucleus (red) were labeled for analyses, with measurements limited to only those cells with a clear nucleus surrounded by cell membrane. (f) Quantitative analysis of myocyte cross-sectional area in NTG-sham (n = 4), NTG-TAC (n = 7), AKT-sham (n = 3), and AKT-TAC (n = 8) mice. Cross-sectional area of 100 cells was measured in the LV-free walls of each animal. Calculations of LV mass (g), myocyte volume (h), and myocyte number (i) from mice 14 wk after TAC based on morphometric analyses of heart as described in Methods. LV mass is significantly increased in both NTG and AKT hearts in the chronic remodeling phase with cell volume of myocytes increasing significantly in the NTG-TAC but not in the AKT-TAC hearts. Myocyte number in the AKT-TAC heart is increased relative to the NTG-TAC, indicating that AKT-TAC myocardium possesses more numerous but smaller myocytes. n = 5 for all morphometric calculation groups except for NTG-TAC, where n = 3 because of increased mortality. ∗, P < 0.05 for comparisons between paired sets of samples as shown.

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