Abstract
Small-for-gestational-age (SGA) infants are fetuses that have not reached their genetically programmed growth potential. Low birth weight predisposes these infants to an increased risk of developing cardiovascular, metabolic and neurodevelopmental conditions in later life. However, our understanding of how this pathology occurs is currently incomplete. Previous research has focused on understanding the transcriptome, epigenome and bacterial signatures separately. However, we hypothesise that interactions between moderators of gene expression are critical to understanding fetal growth restriction. Through a review of the current literature, we identify that there is evidence of modulated expression/methylation of the placental genome and the presence of bacterial DNA in the placental tissue of SGA infants. We also identify that despite limited evidence of the interactions between the above results, there are promising suggestions of a relationship between bacterial signatures and placental function. This review aims to summarise the current literature concerning fetal growth from multiple avenues and propose a novel relationship between the placental transcriptome, methylome and bacterial signature that, if characterised, may be able to improve our current understanding of the placental response to stress and the aetiology of growth restriction.
Highlights
The placenta is the hypomethylated, transitional organ that supports the growth of the developing fetus throughout gestation
An RNA-sequencing study was completed by Sõber et al, 2015 [35] using human placentae collected from pregnancies resulting in SGA infants with and without pre-eclampsia to characterise gene expression changes associated with fetal growth
This study identified the similar expression pattern of genes between late-onset pre-eclampsia (LO-PE) with intrauterine growth restriction (IUGR) and SGA alone as well as LO-PE without IUGR to placentas from pregnancies where the infant was large for gestational age (LGA)
Summary
The placenta is the hypomethylated, transitional organ that supports the growth of the developing fetus throughout gestation. This review investigates the interactions of moderators of placental gene expression in the context of fetal growth restriction and the potential role of bacterial DNA in the regulation process. Assessment of transitional, acute or chronic exposure of the fetus to bacteria and bacterial components during gestation has largely failed to demonstrate causality in adverse fetal outcomes. Recent technological advances have enabled a more integrative analysis of complex data [2,3]. We propose that a more integrative approach to data analysis is more representative of the complexity of a biological system, and that such investigations may lead to an improved understanding of the role of bacterial components in pregnancy outcomes
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