Prostaglandins enhance the synthesis of glycosaminoglycans and inhibit the growth of rabbit aortic smooth muscle cells in culture.
The aim of this study was to elucidate whether prostaglandins (PGs) could be mediators of some of the early changes in atherogenesis. The effect of PGs E1, E2, F1 alpha and F2 alpha on the synthesis of glycosaminoglycans (GAGs) (incorporation of 3H-glucosamine into GAGs) and on the esterification of lipids (incorporation of 3H-oleic acid into lipids) and on cell proliferation (uptake of 3H-thymidine by the cells) was tested in cultured smooth muscle cells. All the PGs studied enhanced the incorporation of 3H-glucosamine into sulphated GAGs with a maximum stimulation at a concentration of 10(-5) mol/l. The synthesis of hyaluronic acid was less clearly increased. The PGs had no effect on cholesterol esterification and they inhibited the uptake of 3H-thymidine by the cells, PGE1 having greatest effect. It was concluded that PGs are not likely mediators of the enhance cell growth or cholesterol esterification in early atherogenesis, but they may contribute to the formation of atherosclerotic lesions by enhancing the synthesis of sulphated GAGs.
D000818:Animals; D001011:Aorta; D002455:Cell Division; D002478:Cells, Cultured; D006025:Glycosaminoglycans / Q000096:biosynthesis*; D009131:Muscle, Smooth, Vascular / Q000166:cytology*; D009829:Oleic Acids / Q000378:metabolism; D011453:Prostaglandins / Q000378:metabolism*; D011817:Rabbits
D006025:Glycosaminoglycans; D009829:Oleic Acids; D011453:Prostaglandins