Altered focal adhesion regulation correlates with cardiomyopathy in mice expressing constitutively active rac1
J. Clin. Invest. Mark A. Sussman, et al. 105:875 doi:10.1172/JCI8497 [
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Figure 2Gross morphology of dilated and hypertrophic racET hearts. (Top) Bisected racET hearts ranging from 7 to 15 days of age (bottom row) compared with typical ntg control hearts shown at 9, 12, and 15 days for comparison (top row). Ntg control hearts show a progressive increase in heart size consistent with rapid postnatal growth in this period. In comparison, racET hearts are enlarged with severely dilated chambers and thin ventricular walls. Atria are also increased in size relative to ntg controls, although to a lesser degree than ventricles. (Middle) Postnatal thyroid hormone supplementation correlates with development of racET cardiomyopathy. Hearts from ntg control mice developed normally without apparent morphologic effects from supplementation (left, shown at 2 weeks of age). In contrast, hearts from supplemented racET mice all developed lethal dilated cardiomyopathy within 1.5 weeks after birth. (Bottom) Bisected hearts ranging from 3 weeks to 6 months of age for ntg controls (top row) and racET mice (bottom row). Concentric hypertrophy is evident in the 3-week-old racET ventricles, but hypertrophic characteristics diminish as the mice age. In contrast, atria in racET mice show severe enlargement by 2 months after birth and continued deterioration as the mice age.
