Defects in nuclear structure and function promote dilated cardiomyopathy in lamin A/C–deficient mice
J. Clin. Invest. Vesna Nikolova, et al. 113:357 doi:10.1172/JCI19448 [Go to this article.]

Figure 2
In vivo analyses of cardiac function with micromanometry and sonomicrometry in mice aged 4–6 weeks. (a) Representative LV pressure-volume loops recorded at steady state are shown for WT (blue), Lmna^+/– (green), and Lmna^–/– (red) mice. Steady-state LV end-diastolic pressure (EDP) plotted against LV end-diastolic volume (EDV) (b) and stress-strain relationships (c) for WT (diamonds, n = 9) Lmna^+/– mice (squares, n = 11), and Lmna^–/– mice (triangles, n = 6). Volume data are normalized to body weight; data are shown as mean ± SD. Functional and morphologic characteristics of cardiac myocytes isolated from mice aged 4–6 weeks were also assessed. (d) Representative recordings of Ca²⁺ transients (top panel) and shortening (lower panel) in single myocytes. Intracellular Ca²⁺ concentration was measured as the change in the 405:485 nm emission ratio for Indo-1. 0.25 represents the magnitude of the Ca²⁺ transient. Lmna^–/– myocytes have similar baseline and peak intracellular Ca²⁺ concentrations to WT and Lmna^+/– myocytes but significantly reduced shortening. (e) Lmna^–/– myocytes are shorter and thinner than WT and Lmna^+/– myocytes but the length/width ratios are similar. Scale bar: 20 μm.