Figure 1. Endocardial-specific deletion of Tie2 results in abnormal trabeculation.

(A–D) Gross images of Tie2^+/fl (A and C) and Tie2-cko (B and D) embryos, lungs, and hearts at E13.5, showing the perivascular hemorrhage, edema (arrow), and pulmonary congestion (arrows) in the mutant embryos. Arrowhead indicates formation of the ventricular groove in the control heart (C), which is usually not obvious in the mutants (D). (E and F) H&E–stained heart sections of E13.5 Tie2^+/fl (E) and Tie2-cko (F) embryos. Arrows indicate trabeculae. (G and H) Tie2^+/fl and Tie2-cko ventricular sections were stained with troponin T (myocardial marker) and endomucin (endocardial marker) antibodies. Compared with the control (Tie2^+/fl), the mutant heart had fewer but thicker trabeculae (arrowheads), thinner compact myocardium, and ventricular septation defects (*). The boxed regions are enlarged in I and J. The width of the ventricular compact wall is indicated. LA, left atrium; Lu, lung; LV, left ventricle; RA, right atrium; RV, right ventricle. Scale bars: I and J, 50 μm; others, 100 μm. A representative of more than 10 images was chosen for each panel. (K–N) Quantification of trabecular myocardium complexity (trabeculae density, trabeculae thickness, and ratio of trabecular layer and compact zone) and compact myocardium thickness from E9.5–E13.5 (n = 6 per group). Data are expressed as mean ± SEM. *P < 0.05; **P < 0.01, 2-way ANOVA.