title: Methylation levels at IGF2 and GNAS DMRs in infants born to preeclamptic pregnancies.
abstract: BACKGROUND
  Offspring of pregnancy complicated with preeclampsia are at high risk for hypertension, stroke and possibly obesity. The mechanisms behind the association of intrauterine exposure to preeclampsia and high risk of health problems in the later life remain largely unknown. The aims of the current investigation were to determine the changes in DNA methylation at IGF2 and GNAS DMR in offspring of preeclamptic pregnancy and to explore the possible mechanisms underlying the association between maternal preeclampsia and high risk for health problems in the later life of their offspring.
  
  
  RESULTS
  Umbilical cord blood was taken from infants born to women of preeclampsia (n=56), gestational hypertension (n=23) and normal pregnancy (n=81). DNA methylation levels of IGF2 and GNAS DMR were determined by Massarray quantitative methylation analysis. Methylation levels at IGF2 DMR were significantly lower in preeclampsia than normal pregnancy. The average methylation level at IGF2 DMR was significantly correlated with preeclampsia even after birth weight, maternal age, gestational age at delivery and fetal gender were adjusted. The difference in methylation level was not significantly different between mild and severe preeclampsia. The methylation level at GNAS DMR was not significantly correlated with birth weight, maternal age, gestational age at delivery, fetal gender, preeclampsia or gestational hypertension.
  
  
  CONCLUSIONS
  We concluded preeclampsia induced a decrease in methylation level at IGF 2 DMR, and this might be among the mechanisms behind the association between intrauterine exposure to preeclampsia and high risk for metabolic diseases in the later life of the infants.
authors.affiliation: Women's Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang Province 310006, China.
authors.forename: Jing
authors.initials: J
authors.lastname: He
authors.forename: Aiping
authors.initials: A
authors.lastname: Zhang
authors.forename: Min
authors.initials: M
authors.lastname: Fang
authors.forename: Rong
authors.initials: R
authors.lastname: Fang
authors.forename: Jiamei
authors.initials: J
authors.lastname: Ge
authors.forename: Yuan
authors.initials: Y
authors.lastname: Jiang
authors.forename: Hong
authors.initials: H
authors.lastname: Zhang
authors.forename: Cong
authors.initials: C
authors.lastname: Han
authors.forename: Xiaoqun
authors.initials: X
authors.lastname: Ye
authors.forename: Danqing
authors.initials: D
authors.lastname: Yu
authors.forename: Hefeng
authors.initials: H
authors.lastname: Huang
authors.forename: Yun
authors.initials: Y
authors.lastname: Liu
authors.forename: Minyue
authors.initials: M
authors.lastname: Dong
mesh_terms: D000328:Adult; D002318:Cardiovascular Diseases / Q000175:diagnosis / Q000235:genetics; D002864:Chromogranins; D019175:DNA Methylation; D005260:Female; D019205:GTP-Binding Protein alpha Subunits, Gs / Q000235:genetics*; D006801:Humans; D046110:Hypertension, Pregnancy-Induced; D007223:Infant; D007335:Insulin-Like Growth Factor II / Q000235:genetics*; D008297:Male; D009035:Mothers; D011225:Pre-Eclampsia; D011247:Pregnancy; D012306:Risk
chemical_list: D002864:Chromogranins; C035170:IGF2 protein, human; D007335:Insulin-Like Growth Factor II; C406732:GNAS protein, human; D019205:GTP-Binding Protein alpha Subunits, Gs