Loss of imprinting and aberrant methylation of IGF2 in placentas from pregnancies complicated with fetal growth restriction

Int J Mol Med. 2011 Oct;28(4):481-7. doi: 10.3892/ijmm.2011.754. Epub 2011 Jul 19.

Abstract

The objective of this study was to investigate the hypothesis that the altered epigenetic mechanisms that regulate IGF2 imprinting in placentas from fetal growth restricted (FGR) pregnancies affect IGF2 expression leading to impaired fetal growth. We investigated gene transcription, genotyping and the methylation patterns of IGF2 from 31 and 17 placentas from FGR-complicated and normal pregnancies, respectively. A statistically significant decrease in IGF2 mRNA levels was observed in the placentas from the FGR pregnancies. Loss of imprinting (LOI) was only detected in the abnormal placentas. The evaluation of the percentage of the methylated reference (PMR) of two different potentially differentially methylated regions (DMR) demonstrated significant PMR values in both sites for the normal and FGR pregnancies with no significant differences. Our results suggest the involvement of the IGF2 imprinted gene in placental function and fetal growth and the possible association of epigenetic alterations with the pathophysiology of fetal growth restriction.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • DNA Methylation / genetics
  • Female
  • Fetal Growth Retardation / genetics*
  • Genomic Imprinting / genetics
  • Genotype
  • Humans
  • Insulin-Like Growth Factor II / genetics*
  • Placenta / metabolism*
  • Pregnancy
  • Reverse Transcriptase Polymerase Chain Reaction

Substances

  • Insulin-Like Growth Factor II