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Ablation of placental REST deregulates fetal brain metabolism and impacts gene expression of the offspring brain at the postnatal and adult stages (snRNA-seq)

ABSTRACT: The Repressor Element-1 Silencing Transcription (REST) factor is a transcriptional repressor. The aim of this study is to characterize role of REST in placental influences on offspring brain. REST was ablated in mouse placenta by mating mouse carrying floxed (FL) alleles of REST with mouse that expresses Cre recombinase under the control of the promoter of placenta-specific gene Gcm1 (glial cells missing 1). To investigate placental influence on gene expression of adult offspring brain cells, single-nuclei RNA-seq was performed. Data analysis showed that ablation of placental REST significantly impacted specific pathways in choroid plexus and ependymal cells of the offspring brain.

ORGANISM(S): Mus musculus

PROVIDER: GSE237181 | GEO | 2024/04/19

REPOSITORIES: GEO

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Ablation of placental REST deregulates fetal brain metabolism and impacts gene expression of the offspring brain at the postnatal and adult stages

Project description:In this study, the transcriptional repressor REST (Repressor Element 1 Silencing Transcription factor) was ablated in the mouse placenta to investigate molecular and cellular impacts on the offspring brain at different life stages. Ablation of placental REST deregulated several brain metabolites, including glucose and lactate that fuel brain energy, vitamin C (ascorbic acid) that functions in the epigenetic programming of the brain during postnatal development, and glutamate and creatine that help the brain to respond to stress conditions during adult life. Bulk RNA-seq analysis showed that a lack of placental REST persistently altered multiple transport genes, including those related to oxygen transportation in the offspring brain. While metabolic genes were impacted in the postnatal brain, different stress response genes were activated in the adult brain. DNA methylation was also impacted in the adult brain due to the loss of placental REST, but in a sex-biased manner. Single-nuclei RNA-seq analysis showed that specific cell types of the brain, particularly those of the choroid plexus and ependyma, which play critical roles in producing cerebrospinal fluid and maintaining metabolic homeostasis, were significantly impacted due to the loss of placental REST. These cells showed significant differential expression of genes associated with the metabotropic (G coupled protein) and ionotropic (ligand-gated ion channel) glutamate receptors, suggesting an impact of ablation of placental REST on the glutamatergic signaling of the offspring brain. The study expands our understanding of placental influences on the offspring brain.

2024-04-19 | GSE236711 | GEO

Insights into the regulation of the brain-placental axis (ChIP-seq)

Project description:Fetal sex influences the accessibility of the placental chromatin to REST. REST targeted fewer sites in the female placental compared to that of male. REST bound to 7,254 common sites in both sexes but nearly 17-fold more number of sites in the male placenta compared to the female placenta.

2023-09-01 | GSE157552 | GEO

Association of dysfunctional synapse defective 1 (SYDE1) with restricted fetal growth – SYDE1 regulates placental cell migration and invasion

Project description:In this study, we identify SYDE1 as a novel GCM1 target gene. We demonstrate that SYDE1 promotes placental cell migration and invasion and that the GCM1-SYDE1 axis is crucial for placental development. Importantly, retarded placental and fetal growth with defective spongiotrophoblast layer, compromised vasculogenesis, and abnormal maternal-trophoblast interface are noted in the Syde1 homozygous knockout (KO) placenta. Along this line, decreased SYDE1 expression is observed in human IUGR placentas. We further demonstrated that components of the renin-angiotensin system (RAS) and Syde2 are differentially expressed in Syde1-KO placenta, which might contribute to normal neonatal delivery in Syde1-KO mothers

2016-10-18 | GSE81468 | GEO

Impact of Maternal Immune Activation and Sex on Placental and Fetal Brain Cytokine and Gene Expression Profiles in a Preclinical Model of Neurodevelopmental Disorders

Project description:Maternal inflammation during gestation is associated with a later diagnosis of neurodevelopmental disorders including autism spectrum disorder (ASD). However, the specific impact of maternal immune activation (MIA) on placental and fetal brain development remains insufficiently understood. This study aimed to investigate the effects of MIA by analyzing placental and brain tissues obtained from the offspring of pregnant dams exposed to polyinosinic:polycytidylic acid (Poly I:C) on embryonic day 12.5. Cytokine and mRNA content in the placenta and brain tissues were assessed using multiplex cytokine assays and bulk-RNA sequencing on embryonic day 17.5. Bulk-RNA sequencing was performed on placenta and brain tissues on embryonic day 17.5.

2024-05-15 | GSE248222 | GEO

Placental effects on maternal brain revealed by disrupted placental gene expression in mouse hybrids

Project description:The mammalian placenta is both the physical interface between mother and fetus, and the source of endocrine signals that target the maternal hypothalamus, priming females for parturition, lactation and motherhood. Despite the importance of this connection, the effects of altered placental signaling on the maternal brain are understudied. Here, we show that placental dysfunction alters gene expression in the maternal brain, with the potential to affect maternal behavior. Using a cross between the house mouse and the Algerian mouse in which hybrid placental development is abnormal, we sequenced late gestation placental and maternal medial preoptic area transcriptomes and quantified differential expression and placenta-maternal brain co-expression between normal and hybrid pregnancies. The expression of Fmn1, Drd3, Caln1 and Ctsr was significantly altered in the brains of females exposed to hybrid placentas. Most strikingly, expression patterns of placenta-specific gene families and Drd3 in the brains of house mouse females carrying hybrid litters matched those of female Algerian mice, the paternal species in the cross. Our results indicate that the paternally-derived placental genome can influence the expression of maternal-fetal communication genes, including placental hormones, suggesting an effect of the offspring's father on the mother’s brain.

2019-12-31 | GSE126469 | GEO

Maternal antioxidant treatment prevents the adverse effects of prenatal stress on the offspring's brain and behavior [NanoString nCounter rat miRNA]

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

Infection of the murine placenta by Listeria monocytogenes induces sex-specific responses in the fetal brain

Project description:BACKGROUND: Epidemiological data indicate that prenatal infection is associated with an increased risk of several neurodevelopmental disorders in the progeny. These disorders display sex differences in presentation. The role of the placenta in the sex-specificity of infection-induced neurodevelopmental abnormalities is not well-defined. We used an imaging-based animal model of the bacterial pathogen Listeria monocytogenes to identify sex-specific effects of placental infection on neurodevelopment of the fetus. METHODS: Pregnant CD1 mice were infected with a bioluminescent strain of Listeria on embryonic day 14.5 (E14.5). Excised fetuses were imaged on E18.5 to identify the infected placentas. The associated fetal brains were analyzed for gene expression and altered brain structure due to infection. The behavior of adult offspring affected by prenatal Listeria infection was analyzed. RESULTS: Placental infection induced sex-specific alteration of gene expression patterns in the fetal brain and resulted in abnormal cortical development correlated with placental infection levels. Furthermore, male offspring exhibited abnormal social interaction, whereas females exhibited elevated anxiety. CONCLUSION: Placental infection by Listeria induced sex-specific abnormalities in neurodevelopment of the fetus. Prenatal infection also affected the behavior of the offspring in a sex-specific manner.

2022-09-22 | GSE213619 | GEO

Serotonin transporter-dependent histone serotonylation in placenta contributes to the neurodevelopmental transcriptome [RNA-seq]

Project description:Brain development requires appropriate regulation of serotonin (5-HT) signaling from distinct tissue sources across embryogenesis. At the maternal-fetal interface, the placenta is thought to be an important contributor of offspring brain 5-HT and is critical to overall fetal health. Yet, how placental 5-HT is acquired, and the mechanisms through which 5-HT influences placental functions, are not well understood. Recently, our group identified a novel epigenetic role for 5-HT, in which 5-HT can be added to histone proteins to regulate transcription, a process called H3 serotonylation. Here, we show that H3 serotonylation undergoes dynamic regulation during placental development, corresponding to gene expression changes that are known to influence key metabolic processes. Using transgenic mice, we demonstrate that placental H3 serotonylation largely depends on 5-HT uptake by the serotonin transporter (Sert/Slc6a4). Sert deletion robustly reduces enrichment of H3 serotonylation across the placental genome, and disrupts neurodevelopmental gene networks in offspring brain tissues. Thus, these findings suggest a novel role for H3 serotonylation in coordinating placental transcription at the intersection of maternal physiology and offspring brain development.

2024-01-23 | GSE246539 | GEO

Serotonin transporter-dependent histone serotonylation in placenta contributes to the neurodevelopmental transcriptome [ChIP-seq]

2024-01-23 | GSE246538 | GEO

Fetal liver programming induced by placental endocrine malfunction

Project description:The placenta acts as an interface between the mother and fetus, regulating nutrient transport and secreting hormones which impact maternal metabolism. Complications during pregnancy, such as placental endocrine malfunction, programme offspring to develop metabolic disease during adulthood, in part via changes in gene expression in critical metabolic organs, such as the liver, during fetal development. Placental endocrine malfunction was induced via the misexpression of two imprinted genes (Igf2 and H19) exclusively in the endocrine zone of the mouse placenta, to study the consequences this has on fetal hepatic gene expression.

2023-11-30 | E-MTAB-11457 | biostudies-arrayexpress

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