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Homocysteine is a risk factor for vascular diseases such as atherosclerosis, and proteoglycans (PGs) derived from arterial smooth muscle cells are the key molecules in atherosclerosis progression. We investigated the effect of homocysteine on the synthesis of PGs in vascular smooth muscle cells in vitro. Homocysteine significantly de- creased the accumulation of PGs, particularly in the conditioned medium, independent of cell density without non- specific cell damage. DEAE-Sephacel ion exchange chromatography of PGs showed that homocysteine selectively decreases chondroitin/dermatan sulfate PG s( CS/DSPGs) with low charge density,i.e. ,t he small CS/DSPG biglycan and decorin, in the conditioned medium. Fluorophore-assisted carbohydrate electrophoresis analysis demonstrated that homocysteine selectively increases the disaccharide unit of iduronic acid-4-O-sulfated N-acetylgalactosamine in chondroitin/dermatan sulfate chains. However, no change was observed in heparan sulfate chains. Therefore, it is suggested that homocysteine inhibits the synthesis of small CS/DSPGs with low charge density in vascular smooth muscle cells. Furthermore, homocysteine affects the microstructure of the chondroitin/dermatan sulfate chains. These alterations may influence the progression of atherosclerosis.

Homocysteine Inhibits Proteoglycan Synthesis in Cultured Bovine Aortic Smooth Muscle Cells