Abstract
The present study aimed to examine the effect of peroxiredocin 1 (Prx1) on vascular smooth muscle cell (VSMC) proliferation, invasion and migration abilities, and to examine the effect of Toll‑like receptor 4 (TLR4) gene silencing on VSMC proliferation, invasion and migration induced by the overexpression of Prx1. The expression of Prx1 in rats with vein graft intimal hyperplasia (IH) was detected using western blot analysis. In addition, VSMCs were retrovirally transfected to establish stable cell lines overexpressing Prx1. An MTT assay was used to determine the effect of the overexpression of Prx1 on VSMC proliferation. A Transwell assay was used to detect the effect of the overexpression of Prx1 on the invasion of VSMCs and a wound‑healing assay was used to determine the effect of the overexpression of Prx1 on the migration of VSMCs. The Prx1‑overexpressed cells were then transfected with interference plasmids of TLR4, to detect the effect of silencing the TLR4 gene on the proliferation and migration of VSMCs using MTT and wound‑healing assays. The results showed that the expression of Prx1 (1.067±0.03) in the IH group was significantly higher, compared with that in the control (0.677±0.05). The number of VSMCs able penetrated the membrane in Prx1-overexpressed group (150±17/visual field) was significantly higher, compared with that in the control (40±5/visual field). The VSMCs in the Prx1‑overexpressed group possessed significantly higher migration ability, compared with those in the control group. The numbers of viable cells in the Prx1‑overexpression groups were 5.625±0.1x105, 8.9±0.737x105 and 10.635±0.065x105, respectively, on days 1, 2 and 3 post‑transfetion, which were significantly higher, compared with those in the control group (3.0±0.025x105, 4.1±0.035x105 and 5.06±0.023x105. The overexpression of Prx1 promoted the proliferation, invasion and migration abilities of the VSMCs. Silencing of the TLR4 gene attenuated the Prx1‑induced proliferation and migration of the VSMCs. Therefore, the promotion of VSMC proliferation and migration by Prx1 was dependent on TLR4, which may become a novel target in the diagnosis, treatment and prognosis of patients with IH.