The differential impact of maternal age on heart, brain, face, and placental development
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ABSTRACT:
PROVIDER: PRJNA861138 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR20396118_1.fastq.gz | Fastqsanger.gz | |||
| SRR20396118_2.fastq.gz | Fastqsanger.gz | |||
| SRR20396119_1.fastq.gz | Fastqsanger.gz | |||
| SRR20396119_2.fastq.gz | Fastqsanger.gz | |||
| SRR20396120_1.fastq.gz | Fastqsanger.gz |
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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
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Project description:Advanced maternal age is a risk factor for neurodevelopmental disorders in offspring. The present study aimed to investigate differences in placental and fetal head gene expression between old and young C57BL6/J female mice. Conceptuses were collected at E12.5 and processed for transcriptomic mRNA gene expression microarray analyses. The most significant differences between old and young females were found in gene expression of the fetal heads (398 differentially expressed genes, DEG) as compared with the placenta (51 DEG).
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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.
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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.
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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:These analyses set out to evaluate placental genomic and epigenomic signatures in newborns from the Extremely Low Gestational Age Newborns (ELGAN) cohort. Genome-wide mRNA, microRNA, and DNA methylation profiles were obtained from placenta samples collected at birth. Analyses were conducted to better understand placental molecular signatures and relate these to placental, maternal, infant, and later-in-life health indices.
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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:Ageing is a crucial factor that affects embryonic development and implantation. Maternal age has an impact on the blastocyst's gene expression levels from the fertilised oocyte and throughout the development of the preimplantation embryo. The current study reported differential gene expression analysis among trophectoderm samples that derived from young maternal age women (YMA - below 30 years), intermediate maternal age (IMA - 30-39 years old) and advanced maternal age women (AMA - at least 40 years old). The molecular approach was assayed by a low-input next generation RNA sequencing approach. Hundreds of significantly differentially expressed transcripts were reported. Extracellular exosome-related transcripts were significantly higher in the trophectoderm cells that derived from young women. According to our analysis, several important transcripts were reported. These molecular biomarkers may have a potential role in embryonic-endometrial communication and could be used in a diagnostic setting, that could help to improve the blastocyst implantation potential.
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