关键词: 低密度脂蛋白受体, DNA甲基化, 同型半胱氨酸, 血管平滑肌细胞

Abstract: Abstract：Objective To explore the mechanism of LDLR methylation in the proliferation of vascular smooth muscle cells induced by homocysteine. Methods 50, 100, 200, 500 μmol/L Hcy were added into the primary cultured VSMCs for 72 hours. MTT was used for the evaluation of VSMCs proliferation viability; the levels of ox-LDL were measured by ELISA; DNA methyltransferase activity was measured by isotope method; the expression of LDLR was detected by Real-time PCR; we examined the promoter DNA methylation status of LDLR by nMS-PCR. Results As the increasing concentrations of Hcy, the levels of ox-LDL and DNA methyl- transferase activity show significant elevation while the proliferation viability of VSMCs were decreased. The mRNA levels of LDLR were increased. nMS-PCR showed that the promoter staus of LDLR were hypomethylated. Compared with the control group, there were significant differences (P<0.05, P<0.01). Conclusion The promoter hypomethylation of LDLR which resulted in the increase of the LDLR expression by Hcy may be one important mechanism of VSMCs injury.

Key words: LDLR, DNA methylation, homocysteine, Vascular smooth muscle cells