Alteration in methylation level at 11β-hydroxysteroid dehydrogenase type 2 gene promoter in infants born to preeclamptic women
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  • 作者:Wensheng Hu ; Xiaoling Weng ; Minyue Dong ; Yun Liu ; Wenjuan Li ; Hefeng Huang
  • 关键词:Preeclampsia ; Offspring ; DNA methylation ; Promoter ; HSD11B2 ; Metabolic diseases
  • 刊名:BMC Genetics
  • 出版年:2014
  • 出版时间:December 2014
  • 年:2014
  • 卷:15
  • 期:1
  • 全文大小:315 KB
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  • 刊物主题:Life Sciences, general; Animal Genetics and Genomics; Microbial Genetics and Genomics; Plant Genetics & Genomics; Genetics and Population Dynamics;
  • 出版者:BioMed Central
  • ISSN:1471-2156
文摘
Background Preeclampsia reduces placental expression and activity of 11β-hydroxysteroid dehydrogenase type 2 (HSD11B2), leading to an increase in fetal glucocordicoids. The latter has been proposed to be associated with low birth weight and high risk of metabolic diseases in later life of the offspring. This investigation aims to delineate the alteration in methylation levels at CpG sites of HSD11B2 promoter. Results Methylation levels of HSD9-2, HSD9-3, HSD23-2 and HSD23-3 and the mean methylation level were significantly lower in preeclampsia than in normal pregnancy (P--.002, 0.031, 0.047 and 0.001, respectively and P--.001 in mean). The mean methylation level was significantly correlated with preeclampsia after the adjustment of birth weight, maternal age, gestational age at delivery and fetal gender (r--.325, P--.001). Conclusions Preeclampsia reduced methylation level at fetal HSD11B2 promoter. A positive correlation existed between HSD11B2 promoter methylation and preeclampsia. Our findings suggest that the methyaltion status of HSD11B2 promoter is a potentially accessible biomarker for preeclampsia. However, further studies are required to address the mechanisms of thehypomethylation at HSD11B2 promoter and the significance of the hypomethylation in the development of metabolic diseases of the fetals born to preeclamptic women.

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