The cytoskeleton of arterial smooth muscle cells during development, atheromatosis, and tissue culture.

Arterial smooth muscle cells (SMCs) assume cytoskeletal features of embryonic cells during human and experimental atheromatosis, as well as when placed in culture. The expression of alpha-smooth muscle (SM) actin can be used to monitor these changes. The synthesis of alpha-SM actin is decreased early after plating in cultured cells and early after endothelial lesion in animals. The amount of mRNA for alpha-SM actin is not affected in cultured cells, although it is drastically decreased in the carotid artery after endothelial injury. Heparin does not modify in vivo the early decrease of alpha-SM actin mRNA and synthesis, but, by inhibiting the entry of SMC into the S phase of the cell cycle, it produces an early reinduction of alpha-SM actin.