The maternal microbiome promotes placental development in mice
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA817556 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR18351938.fastq.gz | Fastqsanger.gz | |||
| SRR18351939.fastq.gz | Fastqsanger.gz | |||
| SRR18351940.fastq.gz | Fastqsanger.gz | |||
| SRR18351941.fastq.gz | Fastqsanger.gz | |||
| SRR18351942.fastq.gz | Fastqsanger.gz |
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Project description:The maternal microbiome is an important regulator of gestational health, but how it affects the placenta as the interface between mother and fetus remains unexplored. Here, we show that the maternal gut microbiota supports placental development in mice. Depletion of the maternal gut microbiota restricts placental growth and impairs feto-placental vascularization. The maternal gut microbiota modulates metabolites in the maternal and fetal circulation. Short-chain fatty acids (SCFAs) stimulate cultured endothelial cell tube formation and prevent abnormalities in placental vascularization in microbiota-deficient mice. Furthermore, in a model of maternal malnutrition, gestational supplementation with SCFAs prevents placental growth restriction and vascular insufficiency. These findings highlight the importance of host-microbial symbioses during pregnancy and reveal that the maternal gut microbiome promotes placental growth and vascularization in mice.
| S-EPMC10558122 | biostudies-literature
Project description:Intra-uterine growth restriction (IUGR) and fetal overgrowth increase the risk of postnatal health. Maternal nutrition is the major intrauterine environmental factor that alters fetal weight. However, the mechanisms underlying maternal nutrition affect fetal development is not entirely clear. We developed a pig model and used isobaric tags for relative and absolute quantification (iTRAQ) to investigate alterations in the placental proteome were obtained from gilts in normal-energy-intake (Con) and high-energy-intake (HE) group, respectively.At 90 d of gestation, the heavy fetuses were found at the tubal ends and light fetuses at the cervical ends of the uterus in Con group and the heavy fetuses had higher glucose concentration than the light fetuses. However, a higher uniformity was noted in HE group. Placental promote between these two positions indicated that a total of 78 and 50 differentially expressed proteins were detected in Con and HE group, respectively. In Con group, these proteins related to lipid metabolism (HADHA, AACS, CAD), nutrient transport (GLUT, SLC27A1) and energy metabolism (NDUFV1, NDUFV2, ATP5C1). However, the differentially expressed proteins in HE group were mainly participation in transcriptional and translational regulation and intracellular vesicular transport.
2018-10-26 | PXD004951 | Pride
Project description:Investigating the impact of maternal age on heart, brain, face, and placental development by using RNA-seq to compare these tissues at E10.5 from young vs. aged females
2022-12-24 | GSE209522 | GEO
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
Project description:Maternal obesity is becoming a major health consideration for successful pregnancy outcomes. There is growing proof that maternal obesity has a negative influence on placental development and function, thereby adversely influencing offspring programming and health outcomes. However, the molecular mechanisms underlying these processes are so far poorly understood. We set out to analyse term placenta whole transcriptome in obese (n=5) and normoweight women (n=5), using Affymetrix microarray platform compromising of 50,000 probe sets. Our analysis shows that the placental transcriptome differs between normoweight and obese women. Different processes and pathways among placenta from obese women were dysregulated, including inflammation and immune responses, lipid metabolism, cell death and survival and cancer pathways, vasculogenesis and angiogenesis, and glucocorticoid receptor signaling pathway. Together, this global gene expression profiling approach demonstrates and confirms that maternal obesity creates a unique in utero environment that impairs placental transcriptome.
2017-01-07 | E-MTAB-4541 | biostudies-arrayexpress
Project description:Maternal RNA transcription plays important roles in maintaining vasculature in mouse placental development associated with regulating gene expression, imprinting status and DNA methylation in the Dlk1-Dio3 imprinted domain.
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Project description:Noninvasive prenatal diagnosis currently used does not achieve desirable levels of sensitivity and specificity. Recently, fetal methylated DNA biomarkers in maternal whole blood have been explored for noninvasive prenatal detection. However, such efforts cover only chromosomal aneuploidy; fetal methylated DNA biomarkers for detecting single-gene disease remain to be discovered. To address this issue, we systematically screened significantly hypermethylated genes in fetal tissues compared with maternal blood for noninvasive prenatal diagnosis of various inherited diseases. First, Methylated-CpG island recovery assay combined with CpG island array was performed in four maternal peripheral bloods and their corresponding placental tissues. Subsequently, direct bisulfite sequencing and combined bisulfite restriction analysis (COBRA) were carried out to validate the reliability of methylation microarray analysis. As results, 310 significantly hypermethylated genes in fetal tissues were detected by microarray. Two of five randomly selected hypermethylated genes detected by microarray were confirmed to be hypermethylated in fetal tissue samples by direct bisulfite sequencing. All four randomly selected hypermethylated genes detected by microarray were confirmed to be hypermethylated in five independent amniotic fluid samples and five independent chorionic villus samples from 10 pregnant women by CORBA. In conclusions, We found a lot of hypermethylated genes and methylation sites in fetal tissues, some of which have great potential to be developed into molecular markers for noninvasive prenatal diagnosis of monogenic disorders. Further clinical study is warranted to confirm these findings. Paired experiments, placental tissues vs. maternal peripheral bloods. Biological replicates: 4 placental tissues and 4 correspoding maternal peripheral bloods.
2012-02-22 | E-GEOD-35997 | biostudies-arrayexpress
Project description:Background: Maternal iron deficiency (ID) is associated with poor pregnancy and fetal outcomes. The effect is thought to be mediated by the placenta but there is no comprehensive assessment of placental response to maternal ID. Additionally, whether the influence of maternal ID on the placenta differs by fetal sex is unknown. Objectives: Our primary aim was to identify gene and protein signatures of ID mouse placentas at mid-gestation. A secondary objective was to profile the expression of iron genes in mouse placentas across gestation. Methods: We used a real-time PCR based array to determine the mRNA expression of all known iron genes in mouse placentas at embryonic day (E) 12.5, E14.5, E16.5, and E19.5 (n=3 placentas/time point). To determine the effect of maternal ID, we performed RNA sequencing and proteomics in male and female placentas from ID and iron adequate mice at E12.5 (n=8 dams/diet). Results: In female placentas, six genes including transferrin receptor (Tfrc) and solute carrier family 11 member 2 were significantly changed by maternal ID. An additional 154 genes were altered in male ID placentas. Proteomic analysis quantified 7662 proteins in the placenta. Proteins translated from iron responsive element (IRE) containing mRNAs were altered in abundance; ferritin and ferroportin 1 decreased while TFRC increased in ID placenta. Less than 4% of the significantly altered genes in ID placentas occurred both at the transcriptional and translational levels. Conclusions: Our data demonstrate that the impact of maternal ID on placental gene expression in mice is limited in scope and magnitude at mid-gestation. We provide strong evidence for IRE-based transcriptional and translational coordination of iron gene expression in the mouse placenta. Finally, we discover sexually dimorphic effects of maternal ID on placental gene expression, with more genes and pathways altered in male compared with female mouse placentas.
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Project description:Concentrations of leptin decline during food restriction. This study was designed to test the hypothesis that some of the effects of maternal food restriction on placental development are mediated by the loss of leptin.
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