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胎儿生长受限相关妊娠胎盘印迹丢失和 IGF2 异常甲基化。

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

机构信息

Department of Obstetrics and Gynaecology, University Hospital of Heraklion, Heraklion, Crete, Greece.

出版信息

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.

摘要

本研究旨在探究以下假说

胎儿生长受限(FGR)妊娠胎盘内调控 IGF2 印迹的表观遗传机制发生改变,会影响 IGF2 的表达,从而导致胎儿生长受损。我们分别检测了 31 例 FGR 相关妊娠和 17 例正常妊娠胎盘的基因转录、基因分型和 IGF2 的甲基化模式。结果显示,FGR 妊娠胎盘内 IGF2 mRNA 水平显著降低。仅在异常胎盘组织中检测到印迹丢失(LOI)。对两个不同潜在差异甲基化区域(DMR)的参照甲基化百分比(PMR)评估显示,正常和 FGR 妊娠的两个位点均有显著的 PMR 值,且无显著差异。我们的研究结果提示,IGF2 印迹基因可能参与胎盘功能和胎儿生长,而表观遗传改变可能与胎儿生长受限的病理生理学有关。

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