Abstract
Smooth muscle cells, fibroblasts derived from various kinds of fibers, chondrocytes originating in elastic cartilage and neutrophils are known as cells that produce elastin and repair damaged elastic fibers or regenerate them. It has also been reported that an elastin-like protein is formed from endothelial cell culture. These facts suggest that various factors are involved in the biosynthesis of elastin.
Using the SD-SLC rat, an atherosclerosis model was prepared administering an atherogenic diet and vitamin D2 in order to determine the effects of elastase on the development, progression and regression of atherosclerosis.
At 6 and 9 weeks after initiation of study, the animals were sacrificed and their thoracic and abdominal aortas removed. The media was isolated by the explant method, and a tissue culture was done while determining tissue levels of elastin. Considering that smooth muscle cells from the control group were more active in division, proliferation and swarming than those from the treated group, it seems to stand to reason to assume that biological kinetics of smooth muscle cells differ from the control group to the treated.