Onset of elastogenesis and downregulation of smooth muscle actin as distinguishing phenomena in artery differentiation in the chick embryo.

During development, the arterial system is grossly divided into elastic and muscular vessel types. Apart from local environmental factors, it has been suggested that vascular smooth muscle cell origin (mesoderm or neural crest) is involved in this, as yet poorly understood, arterial differentiation. We describe differentiation of the thoracic arterial system in the chick embryo, using immunohistochemical techniques staining for muscle-specific actin, vinculin and desmin and histological staining to visualise elastin. The initial developmental stages of the vessel wall in all arteries appeared to be highly similar, with all arteries showing peri-endothelial actin and vinculin staining. Major alterations did not occur until the start of elastogenesis, which coincided with complete loss of actin staining from the proximal part of the great arteries. Later in development, however, actin was re-expressed in a subpopulation of medial cells, which also expressed vinculin and desmin. Concomitantly another, nonmuscular, cell type became evident in the great arteries. Transient loss of actin expression and segregation of very distinct cell populations occurred only in vessels prone to elastic development and known to receive a neural crest contribution. In contrast, arteries that developed a muscular phenotype never lost the initially acquired peri-endothelial actin expression. We also show a significant difference in the organisation of elastic fibres between elastic vessels that contain neural crest derivatives and those that do not. The ductus arteriosus still presents as an enigma in the sense that it is the only part of the pharyngeal arch complex that develops a muscular phenotype.