Fig. 6: VOGM-specific EPHB4 variant disrupts developmental angiogenesis.
From: Mutation of key signaling regulators of cerebrovascular development in vein of Galen malformations
Ephb4+/F867L mice were intercrossed. a Number of live born Ephb4+/+ wild-type (WT), Ephb4+/F867L heterozygote (Het), and Ephb4F867L/F867L homozygote (Hom) mice. **p = 0.0046; Chi-squared test (two-sided). b Images of littermate embryos of the indicated genotypes at E10.5. Note abnormal vascularization of the yolk sac, reduced size and distended pericardial sac (arrow) of homozygous Ephb4F867L/F867L embryos. c Mean +/- 1 SEM of embryo length at E10.5 (WT, n = 10; Het, n = 18; Hom, n = 8). ****P < 0.0001; ns, not significant; Student’s two-sample two-sided t-test. d E10.5 yolk sacs were stained with anti-CD31 antibodies to identify vasculature. Images at right are higher magnifications of the boxed areas of images at left. Note hierarchical vascular networks in yolk sacs of wild-type and heterozygous embryos and primitive vascular plexuses in yolk sacs of homozygous Ephb4F867L/F867L embryos that present as classical honeycomb-like structures at higher magnification. e CD31 antibody staining of E9.5 embryos of the indicated genotypes. For each embryo, the right image is a higher magnification of the boxed area in the left image. Arrows show trunk angiogenesis toward the midline in wild-type and heterozygous embryos but not homozygous Ephb4F867L/F867L embryos. Images in (d, e) are representative of at least 2 embryos of each genotype.
