Roc-A Inhibits Proliferation and Migration of Vascular Smooth Muscle Cells by Regulating Autophagy and Reactive Oxygen Species Accumulation
ZHU Hongying1, DUAN Xiaoqing2, WANG Jianbo1*
This study investigated the inhibitory effect of Roc-A on the proliferation and migration of VSMCs (vascular smooth muscle cells) induced by PDGF-BB and the regulatory mechanism. The rat A7r5 cells were stimulated with 25 ng/mL PDGF-BB to establish a cell injury model. The cells were divided into five groups: control group (NC), PDGF-BB model group, PDGF-BB+10 nmol/L Roc-A group, PDGF-BB+25 nmol/L Roc-A group and PDGF-BB+50 nmol/L Roc-A group. The cell viability and proliferation migration ability seperately were measured by CCK8 and Transwell; intracellular EdU admixture and cell cycle level were measured by flow cytometry; reactive oxygen species accumulation was measured by DCFH-DA fluorescent probe; PCNA, LC3B and P62 protein expression levels were measured by Western blot. The results showed that PDGF-BB treatment led to a significant increase in cell viability and promoted cell proliferation and migration. Roc-A treatment down-regulated PDGF-BB-induced cell activity and PCNA expression, and inhibited cell proliferation and migration. The cell cycle was blocked by Roc-A and the proportion of S-phase cells was reduced in a dose-dependent manner. Meanwhile, Roc-A reversed PDGF-BB-induced reactive oxygen species accumulation and the expression of LC3B II and P62 autophagy-related proteins. Both 5 mmol/L 3-MA and 25 nmol/L Roc-A treatments inhibited smooth muscle cell proliferation and migration. This suggests that Roc-A inhibits PDGF-BB-induced proliferation and migration of VSMCs in rats. This inhibitory effect may be mediated by down-regulation of PDGF-BB-induced autophagy and oxidative stress. It implies a therapeutic effect of Roc-A on endothelial proliferation-induced restenosis.
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