Single-nuclei RNA-seq analysis on utero-placental tissues
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1063776 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR27497463.fastq.gz | Fastqsanger.gz | |||
| SRR27497464.fastq.gz | Fastqsanger.gz | |||
| SRR27497465.fastq.gz | Fastqsanger.gz | |||
| SRR27497466.fastq.gz | Fastqsanger.gz | |||
| SRR27497467.fastq.gz | Fastqsanger.gz |
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Project description:Tissues throughout the human body exert finely-tuned specific functions even when there is considerable overlap in the cellular constituents. Even when the major cellular component of tissues is the same – for example in the case of smooth muscle-rich tissues - discrete phenotypes are evident. Yet, the molecular expression profiles underpinning such specialised functionality is often unclear. This presents a challenge for introducing new medicinal therapies for pathophysiologies: can one target what makes tissue functionality unique without producing unwanted effects on the features that are similar. Such a scenario can be considered for the human uteroplacental unit. Ideally, one would like to target complications of pregnancy like pre-eclampsia (hypertension and proteinuria) or spontaneous preterm birth (early activation of parturition) by targeting particular types of smooth muscle tissues (e.g. arteries versus myometrium) without adversely affecting others. This situation is further complicated by the need to consider maternal and fetoplacental circumstances. Three smooth muscle-rich tissues of importance here are myometrium, maternal uterine (myometrial) arteries and placental arteries. Indeed, each display subtly distinct phenotypes suggesting that distinct molecular signatures may underlie these differences. Hence, we aimed to compare expression profiles of these three tissues to identify the underpinning molecular signatures using multi-omics approaches.
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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:Single nuclei RNA-sequencing of the mouse placenta at four developmental stages (E9.5, E10.5, E12.5, E14.5). Supplementary files include the expression matrices for the integrated datasets containing nuclei from E9.5, E10.5, E12.5, and E14.5 and the clustering annotations for either all nuclei (AllStages_AllNuclei) or subclustered trophoblast nuclei (AllStages_TrophoblastNuclei). Processed data as R objects for both AllStages_AllNuclei and AllStages_TrophoblastNuclei are available at https://figshare.com/projects/Single_nuclei_RNA-seq_of_mouse_placental_labyrinth_development/92354
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Project description:Atmospheric pollution is a rising concern in urban areas and a major contributor to people’s mortality, with potential intergenerational consequences. Our aim was to evaluate the effects of exposure of pregnant F0 females to diluted diesel exhaust (DE) on feto-placental development in the second generation (F2). These rabbits were exposed to diluted and filtered DE (E: exposed group) or clean air (C: Control group) for 2h/day, 5days/week by nose-only exposure from 3rd to 27th days post-conception (dpc). Not exposed anymore after birth, female offspring (F1) were mated with control males at adulthood. F2 feto-placental units were collected at 28dpc. Fatty acid profiles were determined from fetal and maternal plasma, maternal liver and placenta by gas chromatography. Placental structure was explored by stereology while placental gene expression was analyzed using a dedicated microarray. At 28dpc, maternal F1 biochemistry was not different between groups, although F1 E females exhibited increased content of hepatic neutral lipid. Similarly the content of lipid was higher in F2 E placentas, mostly by monounsaturated fatty acids while arachidonic acid was reduced. The proportion of n-3 polyunsaturated fatty acids (n-3 PUFA) was increased whereas AA decreased in F2 E fetal plasma compared to Controls. No structural change was observed in placentas between groups. GSEA analysis of transcriptomic data revealed that gene involved in proteasome complex and ubiquitin pathways were up-regulated in E placentas when compared to C placentas, whereas those involved in ion channel or inflammation regulations were down-regulated. In conclusion, in utero exposure of F1 females to DE can affect both placental function and fetal metabolism in the second generation (F2). Placental FA profiles suggest adaptive protective mechanisms against inflammation, through placental storage of non-essential FA and the favored transplacental transfer of n-3 PUFA. The fetal physiological consequences of observed alterations in placental genes involved in protein metabolism and intracellular signaling remain to be determined. In order to evaluate the intergenerational effects to the F2 generation of in utero F1 exposure to DE, we chose the rabbit model because of its hemochorial placenta closer to the human one (Fischer et al 2012; Furukawa, 2014) than those of rodents. The present study follows our recent publication related to the effects of diesel exhaust exposure of rabbit female F0 during gestation on feto-placental development in F1 and F2 generations (Valentino et al., 2016) where we have shown that F2 feto-placental biometry was not disturbed consecutively to the in utero exposure of the F1 generation (Valentino et al., 2016). Nevertheless, these macroscopically normal fetuses had reduced plasma total cholesterol (-25.9%) and non-HDL cholesterol (-26%) associated with an increase in plasma triglycerides concentrations (+25.9%) compared to F2 control group (Valentino et al., 2016). In the present study, placental function in the second generation was explored at a biochemical and molecular levels in order to understand how the placenta contributed to the fetal dyslipidemia without affecting the biometry.
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