Expression of elastin, smooth muscle alpha-actin, and c-jun as a function of the embryonic lineage of vascular smooth muscle cells.

In the avian embryo, vascular smooth muscle cells (VSMC) in the aortic arch (elastic) arteries originate in the neural crest, whereas other VSMC develop from local mesoderm. These two lineages have been shown previously to be significantly different in the timing and expression of the smooth muscle phenotype and in their respective abilities to produce an orderly elastic matrix. Two differing kinds of VSMC also have been shown in mammals. In the experimental absence of neural crest (NC) in the avian embryo, the matrix is spatially disordered. The molecular basis of the difference between the normal NC-VSMC and the surrogate mesodermal (MDM)-VSMC has not previously been investigated. In this study the expression of vascular smooth muscle alpha-actin, tropoelastin, c-fos and c-jun were examined via immunoblotting, immunohistochemistry, Northern blot, and/or transcription run-on assays. Control avian VSMC of NC origin were compared with experimental MDM-derived VSMC that populate the cardiac outflow after surgical ablation of the NC. The results show that, when they are grown under identical conditions in vitro or freshly removed from an embryonic vessel, surrogate MDM-VSMC express about 10 times more alpha-actin and tropoelastin than the normal NC-VSMC; and MDM-VSMC express up to 15 times more c-jun, whereas c-fos was not different. These results show profound heterogeneity in the regulation of VSMC-specific genes that is based in the embryonic lineage of the cells.