Placental DNA methylation at term reflects maternal serum levels of INHA and FN1, but not PAPPA, early in pregnancy

  title={Placental DNA methylation at term reflects maternal serum levels of INHA and FN1, but not PAPPA, early in pregnancy},
  author={Samantha L. Wilson and John D. Blair and Kirsten Hogg and Sylvie Langlois and Peter von Dadelszen and Wendy P. Robinson},
  journal={BMC Medical Genetics},
BackgroundEarly detection of pregnancies at risk of complications, such as intrauterine growth restriction (IUGR) and preeclampsia (PE), is critical for improved monitoring and preventative treatment to optimize health outcomes. We predict that levels of placental-derived proteins circulating in maternal blood reflect placental gene expression, which is associated with placental DNA methylation (DNAm) profiles. As such, placental DNAm profiling may be useful to distinguish pregnancies at risk… 

Mining DNA methylation alterations towards a classification of placental pathologies

Despite large changes observed in EOPE, there were challenges in reproducing genome-wide DNAm hits that are discussed, and DNAm profiling may provide an independent tool to refine clinical/pathological diagnoses into subgroups with more uniform pathology.

Lower S-adenosylmethionine levels and DNA hypomethylation of placental growth factor (PlGF) in placental tissue of early-onset preeclampsia-complicated pregnancies

The hypomethylation state of the placenta in EOPE, which is reflected by lower SAM and PlGF DNA hypometHylation, underlines the possible role of placental DNA hypometrichylated in the pathophysiology of Eope, which needs further investigation.

Review: placental biomarkers for assessing fetal health.

It is emphasized how increased understanding of the underlying placental biology can aid in the interpretation of approaches and development of new biomarkers that can help predict the onset of pregnancy and neonatal health concerns before they manifest.

The significance of the placental genome and methylome in fetal and maternal health

It is concluded that understanding the influence of the placental genome on common placental-mediated pathologies is critical to improving perinatal health outcomes.

Characterizing the hypomethylated DNA methylation profile of nucleated red blood cells from cord blood.

AIM To provide insight into fetal nucleated red blood cell (nRBC) development using genome-wide DNA methylation (DNAm) profiling. MATERIALS & METHODS The DNAm profile (Illumina 450K array) of cord


This review emphasises on the possible mechanisms in placenta like differential expression of proteins, deregulated pathways, DNA methylation changes that contribute to the pathogenesis of IUGR and also explains the various possible treatment modalities for placental repair and development.

Epigenetic Modifications in the Human Placenta



Novel biomarkers in preeclampsia.

Serum profile in preeclampsia and intra-uterine growth restriction revealed by iTRAQ technology.

Evidence for widespread changes in promoter methylation profile in human placenta in response to increasing gestational age and environmental/stochastic factors

The identification of cellular pathways subject to drift in response to environmental influences provide a basis for future studies examining the role of specific environmental factors on DNA methylation pattern and placenta-associated adverse pregnancy outcomes.

Widespread DNA hypomethylation at gene enhancer regions in placentas associated with early-onset pre-eclampsia

There are widespread DNA methylation alterations in EOPET that may be associated with changes in placental function, and this property may provide a useful tool for early screening of such placentas, according to this study.

Improved reporting of DNA methylation data derived from studies of the human placenta

Improved reporting of DNA methylation data will be critical to identify epigenetic-based effects and to better understand the full phenotypic impact of these widely-reported epigenomic changes.

Comparative gene expression profiling of placentas from patients with severe pre-eclampsia and unexplained fetal growth restriction

The current data indicate a common pathophysiology for FGR and pre-eclampsia, leading to an up-regulation of placental anti-angiogenic factors, however, the findings suggest that it may possibly be the excretion of these factors into the maternal circulation through the TP53-mediated early-stage apoptosis of trophoblasts that leads to the maternal symptoms of pre- eClampsia.

Placental Gene Expression Profile in Intrauterine Growth Restriction Due to Placental Insufficiency

IUGR due to placental insufficiency appears to alter placental glucocorticoid metabolism, upregulates inflammatory response in placenta, and shares common pathogenic mechanisms with severe early-onset preeclampsia.

Screening for preeclampsia using first-trimester serum markers and uterine artery Doppler in nulliparous women.

Hypomethylation of the LEP gene in placenta and elevated maternal leptin concentration in early onset pre-eclampsia