Myricitrin inhibits PDGF-BB-stimulated vascular smooth muscle cell proliferation and migration through suppressing PDGFRβ/Akt/Erk signaling.

Abnormal proliferation and migration of vascular smooth muscle cells (VSMCs) and the stimulation of platelet-derived growth factor (PDGF)-BB play major pathological processes involved in the development of cardiovascular diseases. As a result, the use of anti-proliferative and anti-migratory agents for VSMCs offers promise for the treatment of vascular disorders. Myricitrin is a naturally occurring phenolic compound which possesses antioxidant and anti-inflammatory activity. In this study, we investigate the inhibitory effect of myricitrin on PDGF-BB-induced VSMCs proliferation and migration. In accordance with these findings, myricitrin induced the arrest of cell cycle progression at G0/G1 phase. Myricitrin also decreased the expressions of G0/G1 specific regulatory proteins including cyclin D1, cyclin-dependent kinases (CDK) 4, cyclin E and CDK2, as well as increased the expression of p21 in PDGF-BB-induced VSMCs. Moreover, myricitrin inhibited PDGF-BB-induced phosphorylation of PDGFRβ, Akt and Erk1/2. These results suggest that myricitrin plays an important role in prevention of VSMCs proliferation and migration through the G0/G1 cell cycle arrest by PDGF signaling pathway. Thus, myricitrin is effective in reducing atherosclerotic process by blocking proliferation of VSMCs.