Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1015675 | ENA |
REPOSITORIES: ENA
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Project description:Rising ambient temperatures represent an imminent risk to pregnant women and infants. Both maternal malnutrition and heat stress during pregnancy contribute to poor fetal growth, the leading cause of diminished child development in low-resource settings. However, studies explicitly examining interactions between these two important environmental factors are lacking. We leveraged maternal and neonatal anthropometry data from a randomized controlled trial focused on improving preconception maternal nutrition (Women First Preconception Nutrition trial) conducted in Thatta Pakistan, where both nutritional deficits and heat stress are prevalent. Multiple linear regression of ambient temperature and neonatal anthropometry at birth (n = 459) showed a negative association between daily maximal temperatures in the first trimester and z-scores of birth length (LGAZ) and head circumference (HCGAZ). Placental mRNA-sequencing and protein analysis showed transcriptomic changes in protein translation, ribosomal proteins and mTORC1 signalling components in term placenta exposed to excessive heat in the first trimester. Targeted metabolomic analysis indicated ambient temperature associated alterations in maternal circulation with decreases in choline concentrations. Notably, negative impacts of heat on birth length were in part mitigated in women randomized to comprehensive maternal nutritional supplementation (MNS) before pregnancy suggesting potential interactions between heat stress and nutritional status of the mother. Collectively the findings bridge critical gaps in our current understanding of how maternal nutrition may provide resilience against adverse effects of heat stress in pregnancy.
2023-02-08 | GSE220877 | GEO
Project description:Maternal exposure to stress during pregnancy is associated with an increased risk of psychiatric disorders in the offspring in later life. The mechanisms through which the effects of maternal stress are transmitted to the fetus are unclear, however the placenta, as the interface between mother and fetus, is likely to play a key role. Using a rat model, we investigated a role for placental oxidative stress in conveying the effects of maternal social stress to the fetus and the potential for treatment using a nanoparticle-bound antioxidant to prevent adverse outcomes in the offspring. Maternal psychosocial stress increased circulating corticosterone in the mother, but not in the fetuses. Maternal stress also induced oxidative stress in the placenta, but not in the fetal brain. Blocking oxidative stress using an antioxidant prevented the prenatal stress-induced anxiety phenotype in the male offspring, and prevented sex-specific neurobiological changes, specifically a reduction in dendrite lengths in the hippocampus, as well as reductions in the number of parvalbumin-positive neurons and GABA receptor subunits in the hippocampus and basolateral amygdala of the male offspring. Importantly, many of these effects were mimicked in neuronal cultures by application of placental-conditioned medium or fetal plasma from stressed pregnancies, indicating molecules released from the placenta may mediate the effects of prenatal stress on the fetal brain. Indeed, both placenta-conditioned medium and fetal plasma contained differentially abundant microRNAs following maternal stress, and their predicted targets were enriched for genes relevant to nervous system development and psychiatric disorders. The results highlight placental oxidative stress as a key mediator in transmitting the maternal social stress effects on the offspring's brain and behaviour, and offer a potential intervention to prevent stress-induced fetal programming of affective disorders.
2020-12-01 | GSE130573 | GEO
Project description:Congenital cytomegalovirus (cCMV) is the most common intrauterine infection, leading to infant neurodevelopmental disabilities. An improved knowledge of correlates of protection against cCMV is needed to guide prevention strategies. Here, we employed a unique ex vivo model of human CMV (HCMV) infection in decidual tissues of women with and without preconception immunity, recapitulating nonprimary versus primary infection at the authentic maternofetal transmission site. We showed that decidual tissues of women with preconception immunity exhibited intrinsic resistance to HCMV, mounting a rapid activation of tissue resident memory CD8+ and CD4+ T cells upon nonprimary infection. We further revealed the role of HCMV-specific decidual-tissue resident CD8+ T cells in local protection against nonprimary HCMV infection. The findings could inform the development of vaccine against cCMV, and provide insights for further studies of the integrity of immune defense against cCMV and other pathogens in the human maternal-fetal interface.
2024-08-01 | GSE240976 | GEO
Project description:Maternal and fetal monocytes and tissue macrophages (decidual macrophages, Hofbauer cells) at the feto-maternal interface have different methylome.
2011-11-15 | GSE31680 | GEO
Project description:The first trimester is a critical window of maternal-fetal communication for pregnancy. RNA-sequencing of matched maternal decidua (4) and placenta (4) identified 91 sexually dimorphic receptor-ligand pairs across the maternal-fetal interface, 32 in females and 59 in males.
2020-08-20 | GSE131874 | GEO
Project description:Microarray analysis to globally assess gene expression at the maternal-fetal interface Keywords: age
2007-01-11 | GSE5999 | GEO
Project description:The placenta plays a crucial role in the normal growth and development in mammals by serving as an interface for nutrients, respiratory gases and physiological signals between the mother and fetus. Here we use a novel embryo transfer system in mice to identify the major physiological pathways in the placenta that are principally influenced by altered maternal environment. Embryos of identical genotype were transferred at the one cell stage into surrogate mothers either of the same strain or from a different strain. We analyzed the relative effects of maternal and fetal genotype on fetal weight, placental weight and the placental transcriptome at E18.5. The results show that maternal genotype overrides fetal genotype as the principal regulator of fetal weight (p<0.0001). Microarray analysis of the transcriptome in placentas revealed that a small fraction (0.25%) of placental genes are specifically regulated by maternal genotype (p<0.05, FDR<0.10). Pathway analysis of these genes using the programs Gene Ontology and MetaCore from GeneGO inc. revealed highest statistical significance in signaling pathways that regulate cell growth and lipid metabolism. These results provide a mechanistic understanding of important molecular pathways involved in maternal regulation of fetal growth and development.
2010-08-06 | E-MEXP-2479 | biostudies-arrayexpress
Project description:The involvement of epigenetic regulation of cis-regulatory elements and retrotransposons in the maternal-fetal interface of COVID-19-related pregnancy complications.
2023-05-02 | E-MTAB-11749 | biostudies-arrayexpress
Project description:Maternal and fetal monocytes and tissue macrophages (decidual macrophages, Hofbauer cells) at the feto-maternal interface have different methylome. Paired and balanced design. We compared maternal blood monocytes (MB) vs. cord blood monocytes (CB), maternal blood monocytes (MB) vs. decidual macrophages (Deci), cord blood monocytes (CB) vs placental macrophages (villi) and decidual macrophages (Deci) vs. placental macrophages (villi).
2011-11-15 | E-GEOD-31680 | biostudies-arrayexpress
Project description:Fetal alcohol exposure at any stage of pregnancy can lead to Fetal Alcohol Spectrum Disorder (FASD), a group of life-long conditions characterized by congenital malformations, as well as cognitive, behavioral, and emotional impairments. The teratogenic effects of alcohol have long been publicized; yet fetal alcohol exposure is one of the most common preventable causes of birth defects. Currently, alcohol abstinence during pregnancy is the best and only way to prevent FASD. However, alcohol consumption remains astoundingly prevalent among pregnant women; therefore, additional measures need to be made available to help protect the developing embryo before irreparable damage is done. Maternal nutritional interventions using methyl donors have been investigated as potential preventative measures to mitigate the adverse effects of fetal alcohol exposure. Here, we show that a single acute preimplantation (E2.5; 8-cell stage) fetal alcohol exposure in mice leads to long-term FASD-like morphological phenotypes (e.g., growth restriction, brain malformations, skeletal delays) in late-gestation embryos (E18.5) and demonstrate that supplementing the maternal diet with a combination of four methyl donor nutrients, folic acid, choline, betaine, and vitamin B12, prior to conception and throughout gestation effectively reduces the incidence and severity of alcohol-induced morphological defects without altering DNA methylation status and regulation of imprinting control regions. This study clearly supports that preimplantation embryos are vulnerable to the teratogenic effects of alcohol, emphasizing the dangers of maternal alcohol consumption during early gestation, and provides a potential proactive maternal nutritional intervention to minimize FASD progression, reinforcing the importance of adequate preconception and prenatal nutrition.
2023-01-23 | GSE222974 | GEO