Fig. 5. Examination of blood vessel formation and maturation in the head area. (A,C,E,G,I,K) Sections of homozygous C3G mutant embryos at E11.0 and (B,D,F, H,J,L) sections of wild-type littermate controls. A-D,K,L are paraffin sections, E-J are frozen sections. SMA immunostaining for vascular pericytes and smooth muscle cells using horseradish peroxidase histochemistry (A-D) or fluorescent labelling (G,H) and nuclear counterstaining with Methyl Green (A-D) or bis-benzimide (G-J). PECAM 1 immunostaining for vascular endothelial cells (E,F,I,J). Nidogen immunostaining for one of the proteins produced by endothelial cells (K,L). G,I and H,J are neighbouring sections of the basilar artery. Note the reduction of SMA staining in mutant embryos (A,C,G) and the lack of cohesion between the few SMA-positive cells (A). Lack of SMA-staining cells is more complete in small blood vessels (A,C) than in larger blood vessels (G). Arrowheads point to blood vessels and capillaries in C and D. However, even larger blood vessels have fewer SMA-staining cells (G compared with H). In contrast, vascular endothelial cells are unaffected by the C3G mutation. All embryos were alive at the time of tissue preparation. Bar represents 28 µm in A,B, 56 µm in C,D,G,H,I,J and 110 µm in E,F,K,L.

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