Xu Peng, Wu Zhongqiang, Yang Weiwei, Wang Lan
School of Life Science, Shanxi University, Taiyuan 030006, China; Bio-X Institutes, Key Laboratory for the Genetics of Developmental and Neuropsychiatric Disorders (Ministry of Education), Shanghai Jiao Tong University, Shanghai 200030, China.
School of Life Science, Shanxi University, Taiyuan 030006, China.
Toxicology. 2017 Sep 1;390:109-116. doi: 10.1016/j.tox.2017.08.003. Epub 2017 Aug 18.
Cadmium (Cd) is one of the most toxic environmental pollutants that cause fetal malformation and growth restriction. However, the molecular mechanisms underlying maternal Cd toxicity on fetal growth remain largely unknown. Specifically, the expression profiles and the regulation mechanisms of the imprinted genes, have been poorly characterized in the etiology of Cd-induced fetal growth restriction (FGR). In the present study, 13 imprinted genes associated with the fetal growth and placenta development were selected and their expression patterns were examined in the Cd-exposed placentas. Quantitative real-time PCR and western blot results showed that the maternally expressed gene, Cyclin dependent kinase inhibitor 1c (Cdkn1c), and paternally expressed gene, Paternally expressed gene 10 (Peg10), were significantly upregulated and downregulated respectively in the Cd-exposed placentas when compared to the normal ones respectively. Moreover, data from bisulfate PCR demonstrated the changes of the methylation levels of the promoter regions of Cdkn1c and Peg10 in the Cd-exposed placentas. In addition, the expression profile of Cdkn1c was correlated with the methylation levels of site 2 (-837--692) but not site 1 (-389--185) of its promoter region. Therefore, our results suggest that changes of the DNA methylation levels of the promoter regions and the expression patterns of Cdkn1c and Peg10 may be involved in the etiology of Cd-induced fetal growth restriction.
镉(Cd)是最具毒性的环境污染物之一,可导致胎儿畸形和生长受限。然而,母体镉毒性对胎儿生长的分子机制仍 largely 未知。具体而言,印迹基因的表达谱和调控机制在镉诱导的胎儿生长受限(FGR)病因中尚未得到充分表征。在本研究中,选择了 13 个与胎儿生长和胎盘发育相关的印迹基因,并在镉暴露的胎盘中检测了它们的表达模式。定量实时 PCR 和蛋白质印迹结果表明,与正常胎盘相比,镉暴露的胎盘中母源表达基因细胞周期蛋白依赖性激酶抑制剂 1c(Cdkn1c)显著上调,父源表达基因父源表达基因 10(Peg10)显著下调。此外,亚硫酸氢盐 PCR 数据表明镉暴露胎盘中 Cdkn1c 和 Peg10 启动子区域的甲基化水平发生了变化。此外,Cdkn1c 的表达谱与其启动子区域位点 2(-837--692)而非位点 1(-389--185)的甲基化水平相关。因此,我们的结果表明,启动子区域的 DNA 甲基化水平变化以及 Cdkn1c 和 Peg10 的表达模式可能参与了镉诱导的胎儿生长受限的病因。