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Annie Bourdeau, Daniel J. Dumont, Michelle Letarte
Published in Volume 104, Issue 10
J Clin Invest. 1999; 104(10):1343–1351 doi:10.1172/JCI8088
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Figure 3

Vascular defects in End–/– mice. Whole-mount embryos in their yolk sacs were stained for β-gal activity. (a, b, e, and f) Direct microscopic examination of the yolk sacs. (c, d, g, and h) Sagittal histological sections. At E9.0, the normal capillary plexus and initiation of branching are seen in the End+/– embryo (a and c). The End–/– yolk sac also has a highly vascularized plexus, but no vessel branching is observed (b and d). At E9.5, a vitelline vessel (v) is readily detectable in the End+/– yolk sac (e); this intact vessel is full of primitive red cells (g). The End–/– yolk sac shows a disorganized capillary plexus and no vitelline vessels (f); abnormally dilated blood islands are seen (h), which have ruptured, releasing primitive erythroblasts toward the amnion (arrowhead). (i and j) Unstained E9.5 embryos, with yolk sac and placenta still attached. Bleeding in the yolk sac cavity (arrowhead) and edematous pericardium (arrow) are observed in End–/– embryo (j), compared with a littermate control (i). An unstained E9.0 End+/– embryo (k), dissected away from the yolk sac, is compared with an End–/– littermate (l), which shows internal bleeding (arrow). Sagittal sections stained for β-gal demonstrate the presence of blood (arrow) in the peritoneal cavity of the End–/– embryo (n), which is absent from the End+/– embryo (m). a, dorsal aorta; pc, peritoneal cavity; u, umbilical vein. Bar: 100 μm (ah), 500 μm (i and j), 250 μm (kn).