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 3Myocardial histology in mice aged 4–6 weeks. Heart tissue from WT (
a,
d, and
g),
Lmna+/– (
b,
e, and
h), and
Lmna–/– (
c,
f, and
i) mice was evaluated by light microscopy after staining with H&E (
a–
f) and electron microscopy (
g–
i). Cross-sections at the midventricular level (
a–
c) show LV and RV dilation in
Lmna–/– hearts. Scale bar: 1 mm. Higher magnification (
d–
f) shows overall myocardial architecture in
Lmna–/– LV myofibrils is relatively preserved. Nuclear elongation and chromatin dispersion are evident in
Lmna+/– and
Lmna–/– cardiomyocytes (insets). Scale bar: 50 μm. Sarcomere organization (
g–
i) appears normal in all mice. Scale bar: 2 μm.
