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Fig. 6. EphA2-deficiency impairs ephrin-A1-induced angiogenesis in vivo. (A) Sponges impregnated with ephrin-A1 or IgG were subcutaneously implanted into the dorsal flank of EphA2 heterozygous (EphA2+/–) or EphA2-deficient (EphA2–/–) mice. After 7 days, mice were injected intravenously with TRITC-dextran to visualize host blood vessels associated with sponges. Fewer surface vessels were associated with ephrin-A1-treated sponges in EphA^-/– animals relative to EphA^+/– controls. Scale bar, 5 mm. Arrowheads indicate surface blood vessels covering sponges. (B) Sponge sections were counterstained with DAPI to visualize nuclei relative to TRITC vessel labeling. Vessel infiltration in the ephrin-A1-treated sponge periphery was detected in control EphA^+/– animals, but not in EphA^-/– animals. Scale bar, 10 µm. Dashed line indicates the boundary between adjacent host skin tissue (left) and sponge (right). Arrows indicate TRITC-positive vessels that have infiltrated into the sponge, and (^*) indicate vessels within the host skin tissue. (C) Left panel displays higher magnification (40x) of the upper left panel in B. Scale bar, 5 µm. Right panel displays low magnification (10x) of the lower left panel in B, demonstrating the distance of host vessels relative to the boundary of IgG-treated sponges in EphA^+/– animals. Scale bar, 1 mm. Data are a representative of results from three independent mice per genotype.

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