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Figure 4 Heterozygous  E-catenin C-Terminal Deficient Mice Show Susceptibility to Infarct Rupture Post-MI
(A) Kaplan-Meier curve analysis of heterozygous E-catenin C-terminal deficient mice (n = 9) showed significantly lower rupture-free survival post-myocardial infarction (MI) (#p = 0.038) compared with their wild-type littermates (n = 11). (B) Macroscopic image of infarct rupture (T = tweezers). The arrow points at the tear in the infarct area, showing the blood loss through the ventricular wall. (C) Representative images of immunohistochemical analysis of E-catenin, showing less intense staining of the intercalated disks in the heterozygous mice compared with staining in the wild-type littermates. (D to G) (Top) Representative Western blot analysis for E-catenin (D), β-catenin (E),  -catenin (F), and N-cadherin (G) in heterozygous C-terminal E-catenin deficient mice and their wild-type littermates, both from septum (nonischemic) and infarct tissue; β-actin was used for normalization of the samples. (Bottom) Quantitative analysis of adhesion complex proteins, expressed as protein/β-actin ratio, demonstrating significantly lower E-catenin in mice heterozygously deficient for C-terminally truncated E-catenin (n = 9) compared with that in their wild-type littermates (n = 11). The other cell adhesion proteins were unaffected, although N-cadherin showed more degradation under ischemic conditions in the heterozygous mice. *p < 0.01; **p < 0.001; #p < 0.05.
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