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 = 0.002, 0.031, 0.047 and 0.001, respectively and P < 0.001 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 = 0.325, P < 0.001).
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.