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J.Health Sci., 54(1), 56-65, 2008
Homocysteine Inhibits Proteoglycan Synthesis in Cultured Bovine Aortic Smooth Muscle Cells
Yasuyuki Fujiwara,a Chihiro Mikami,b
Michinori Nagai,b Chika Yamamoto,b, c
Takashi Hirooka,c Masahiko Satoh,a
and Toshiyuki Kaji*, b, c
aLaboratory of Pharmaceutical Health Sciences, School of Pharmacy, Aichi Gakuin University, 1-100 Kusumoto-cho, Chikusa-ku, Nagoya, Aichi 464-8650, Japan,
bDepartment of Environmental Health, Faculty of Pharmaceutical Sciences, and
cOrganization for Frontier Research in Preventive Pharmaceutical Sciences, Hokuriku University, Ho-3 Kanagawa-machi, Kanazawa 920-1181, Japan
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 decreased the accumulation of PGs, particularly in the conditioned medium, independent of cell density without nonspecific cell damage. DEAE-Sephacel ion exchange chromatography of PGs showed that homocysteine selectively decreases chondroitin/dermatan sulfate PGs (CS/DSPGs) with low charge density, i.e., the 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.
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