The purpose of this study was to investigate in vitro the potential effect of type 1 collagen gel containing alpha-elastin on the proliferation of vascular smooth muscle cells and vascular endothelial cells, and on smooth muscle cell migration. Vascular smooth muscle cell and endothelial cell were cultured in 12-well plates precoated with collagen gels and alpha-elastin. Cell proliferation rates were measured by monitoring [3H]-thymidine incorporation. After 2, 3 or 4 days of culture, the proliferation rate of both smooth muscle cells and endothelial cells was significantly decreased on collagen gel containing 10 mg/ml alpha-elastin compared with collagen gel only as control. Smooth muscle cell proliferation on collagen gel containing alpha-elastin on the 4th day of culture was decreased dose-dependently, e.g. 1 mg/ml of alpha-elastin (74.8(2.3)% of control, P=n.s.); 5 mg/ml (56.7(2.1)%; P<0.05); 10 mg/ml (30.3(3.1)%; P<0.005). In the case of cultured endothelial cells, however, [3H]-thymidine incorporation was not decreased significantly in the presence of 5 mg/ml alpha-elastin (83.1(7.9)%, P=n.s.). After stimulation by platelet-derived growth factor, the smooth muscle cell migration rate on collagen gel containing alpha-elastin (5 mg/ml) was decreased over time. The area of migration on the 6th day of culture was also significantly decreased dose-dependently in the presence of alpha-elastin, e.g. 1 mg/ml (72.6(3.4)% of control, P<0.05), 5 mg/ml (56.9%(1.5)%; P<0.05); 10 mg/ml (37.3(2.7)%; P<0.0005). In conclusion, alpha-elastin inhibited the proliferation and migration of smooth muscle cell in a dose-dependent manner on collagen gel culture, however, at high concentrations of alpha-elastin (10 mg/ml), the endothelial cell proliferation rate was also inhibited. At 5 mg/ml, alpha-elastin significantly inhibited smooth muscle cell proliferation and migration but did not significantly inhibit endothelial cell proliferation. Incorporation of collagen gel containing alpha-elastin into the structure of arterial prosthesis offers the possibility of inhibiting smooth muscle cell hyperplasia without significant effect on endothelial cell formation.