Fig. 7. Defective smooth muscle integrity in Wnt7b^lacZ–/– embryos and mice. Close examination of blood vessels in wild-type (A, arrow) and Wnt7b^lacZ–/– P0 neonates (B,C) reveals several breaches in the vessel wall in Wnt7b^lacZ–/– mice. In some instances, very little of the structure of the wall is left (B, arrows), while in others a thicker vessel wall with several ruptures is observed (C, arrows). Staining of sections with an antibody against smooth muscle -actin shows robust staining surrounding blood vessels in wild-type neonates (D, arrows). Smooth muscle -actin staining shows reduced staining, suggesting degradation of smooth muscle surrounding some vessels in Wnt7b^lacZ–/– neonates (E, arrows), while other vessels show frank breaches in the hypertrophic vessel wall (F). Bronchial smooth muscle appears normal in both wild-type (G, arrowhead) and Wnt7b^lacZ–/– neonates (H, arrowhead). TUNEL staining shows an increase in TUNEL-positive cells in the smooth muscle of the blood vessel wall in Wnt7b^lacZ–/– neonates (J, arrowhead) but not in bronchial smooth muscle (K, arrow). This is not observed in wild-type littermates (I, arrow). PECAM staining reveals a normal endothelial network in wild-type (L) and Wnt7b^lacZ–/– neonates (M). Many large blood vessels showed rupture of the smooth muscle layer with herniation of the intact endothelial cell layer (N, arrow).