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Modulation of Placental Gene Expression in Small-for-Gestational-Age Infants
Jessica L O'Callaghan1,2, Vicki L Clifton3, Peter Prentis4
1School of Biomedical Sciences, Faculty of Health, Queensland University of Technology, Brisbane 4001, Queensland, Australia.
Insights
Small-for-gestational-age (SGA) infants face lifelong health risks due to restricted fetal growth. This review explores how placental gene expression, methylation, and bacteria interact, potentially explaining SGA development and improving understanding of fetal growth restriction.
Area of Science:
- Perinatal biology
- Fetal development
- Genomics and epigenomics
Background:
- Small-for-gestational-age (SGA) infants exhibit suboptimal fetal growth, increasing risks for cardiovascular, metabolic, and neurodevelopmental issues later in life.
- Current understanding of SGA etiology is limited, with prior research examining placental transcriptome, epigenome, and bacterial signatures in isolation.
Purpose of the Study:
- To review existing literature on fetal growth restriction from multiple perspectives.
- To propose a novel hypothesis integrating placental transcriptome, methylome, and bacterial signatures to explain SGA development.
Main Methods:
- Comprehensive literature review of studies on placental gene expression, methylation, and bacterial presence in SGA infants.
- Analysis of existing evidence for interactions between these factors in the context of fetal growth restriction.
Main Results:
- Evidence indicates altered placental gene expression/methylation and the presence of bacterial DNA in SGA infants.
- Limited but suggestive data points towards a relationship between placental bacterial signatures and placental function.
Conclusions:
- Interactions between placental gene expression, methylation, and bacterial signatures are critical for understanding fetal growth restriction.
- Characterizing these interactions may enhance our comprehension of placental stress responses and the origins of SGA.
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.
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