BPB Reports

Paper Details

BPB Reports
Vol. 2 No. 6 p.106-112 2019
Regular Article
Induction of Versican V0 Variant Synthesis by A Thrombin Receptor Agonist Peptide in Cultured Human Coronary Smooth Muscle Cells
  • Toshiyuki Kaji (Faculty of Pharmaceutical Sciences, Tokyo University of Science / t-kaji@rs.tus.ac.jp)
Takato Hara 1) , Takako Wakata 2) , Yasuyuki Fujiwara 3) , Chika Yamamoto 1) , Toshiyuki Kaji 4)
1) Faculty of Pharmaceutical Sciences, Toho University , 2) Faculty of Pharmaceutical Sciences, Hokuriku University , 3) School of Pharmacy, Tokyo University of Pharmacy and Life Sciences , 4) Faculty of Pharmaceutical Sciences, Tokyo University of Science
Received: November 06, 2019;   Accepted: November 25, 2019;   Released: December 18, 2019
Keywords: atherosclerosis, versican, thrombin, protease-activated receptor, proteoglycan, vascular smooth muscle cell

Versican is a large aggregating chondroitin sulfate proteoglycan that accumulates in vascular wall during atherosclerosis. This proteoglycan is particularly synthesized by arterial smooth muscle cells and contributes to atherosclerosis progression by enhancing the retention of low density lipoproteins and inducing the proliferation and migration of the cells in atherosclerotic plaques. There is a strong interrelationship between atherosclerosis and thrombosis, suggesting that thrombin—a key coagulation factor—may stimulate versican synthesis in arterial smooth muscle cells. To determine the regulation of proteoglycan synthesis by thrombin receptor agonist peptide (SFLLRN), cultured human coronary smooth muscle cells were stimulated by the peptide, and proteoglycans synthesized by the cells were characterized by biochemical techniques. The experiments indicate that SFLLRN enhances the synthesis of versican V0 variant without affecting the length and disaccharide composition of its chondroitin sulfate chains under high cell density condition. This suggests that the procoagulant state of blood may accelerate atherosclerosis progression through a high accumulation of versican V0 variant derived from arterial smooth muscle cells after the cell density becomes higher in atherosclerotic plaques.