关键词: PM2.5, 组蛋白去乙酰化酶, 血管内皮生长因子, 宫内生长受限

Abstract: Objective To investigate the role of histone acetylation in PM2.5 in utero exposure induced intrauterine growth retardation (IUGR). Method Pregnant mice were exposed to PM2.5 during the whole gestation, mice of control group were exposed to normal saline, non-treatment in blank control group; Birth weights were monitored; protein and mRNA levels of histone deacetylase (HDAC1/2/3 and vascular endothelial growth factor (VEGF) were measured by Western blot and Q-PCR methods; fluorometric assay was used to detect the activities of HDAC1/2/3; ChIP-PCR assay was employed to determine the binding levels of HDAC1 and HDAC2 with the promoter region of VEGF. Results Birth weights of mice in PM2.5 exposed group were significantly lower than those in control groups (p<0.05). HDAC1 and HDAC2 expression levels increased in trial groups, compared to controls (p<0.05). Protein and mRNA levels of VEGF decreased in PM2.5 exposed group, compared to those in control groups (p<0.05). Compared with control groups, HDAC2 activities went up after PM2.5 exposure (p<0.05). Binding levels of HDAC2 with promoter of VEGF increased (p<0.05). Conclusions PM2.5 exposure during gestation could induce IUGR, in our model, HDAC2 mediated a hypoacetylation near VEGF’s promoter, which caused a decrease of VEGF in placenta.

Key words: particular matter 2.5, histone deacetylases, vascular endothelial growth factor, intrauterine growth retardation.