1987 Volume 15 Issue 3 Pages 539-543
Quiescent smooth muscle cells (SMC) obtained from atherosclerotic intima of rabbit (intimal SMC) received an atherogenic diet showed different proliferative activity from medial SMC of normal rabbit aorta (medial SMC). Intimal SMC kept high proliferative capacity (saturation density: 6.35±1.83×104 cells/cm2) until at least 30th passage, though normal medial SMC showed lower saturation density (1.12±0.47×104 cells/cm2) and lost growth ability after 4th passage. After an initial lag phase, DNA synthesis of medial SMC in medium containing normal rabbit serum increased rapidly with a maximum after 26 hours. Stimulation with medium containing hyperlipidemic serum did not change the kinetics of DNA synthesis. DNA synthesis of intimal SMC in medium with either normal or hyperlipidemic serum reached maximum rate between 26 and 30 hours after medium change. DNA synthesis of medial SMC stimulated, twice with an interval, by hyperlipidemic serum for 8 or 24 hours was significantly higher than in the control. On the stimulation by hyperlipidemic serum, intimal SMC reacted in a similar fashion to medial SMC. In both medium containing either hyperlipidemic or normal serum, 3H-thymidine uptake of intimal SMC was higher than medial cells. Hyperlipidemic serum did not stimulate further DNA synthesis of both medial and intimal SMC in logarithmic growth phase.
It appeared that enhancement of DNA synthesis by an exposure to hyperlipidemic serum in both medial and intimal SMC did not depend upon the changes of intracellular lipid content during incubation times. However the ratio of phospholipid to free cholesterol seemed to be correlate to the increasing of DNA synthesis.
Insulin in 1 or 5μg/ml concentration stimulated to proliferation of both medial and intimal SMC. However the stimulatory response of intimal SMC was lower than that of medial SMC.
Intimal SMC had more resistibility to the cytotoxic effect of hyperlipidemic serum, measured by the 51Cr-release from cell membrane than medial SMC. It is possible that intimal smooth muscle cells can proliferate intensely without stimulation by specific growth factor and making resistance to the cytotoxic effect of hyperlipidemic serum and induce atherosclerosis.
