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 [
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Figure 1Comparative morphometry in mice aged 4–6 weeks. (
a) When compared with WT (left) and
Lmna+/– littermates (center),
Lmna–/– (right) mice exhibit growth retardation with 50% reduction in body weight. (
b) Despite marked differences in body size, longitudinal sections show that heart sizes are similar in WT (left),
Lmna+/– (center), and
Lmna–/– (right) mice.
Lmna–/– hearts show LV and LA dilation with wall thinning. Scale bar: 2.5 mm. (
c) The phenotype of severe DCM without compensatory hypertrophy in 4- to 6-week-old
Lmna–/– mice is reflected by Northern blot analyses that show appropriate increases in LV expression of ANP and BNP but no induction of β-MHC or α-skeletal actin. +/+, WT; +/–,
Lmna+/–; –/–,
Lmna–/–.
