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GPER1 inhibits placental type I IFN responses to preserve fetal health during maternal infection [RNAseq]

ABSTRACT: GPER1 inhibits placental type I IFN responses to preserve fetal health during maternal infection [RNAseq]

PROVIDER: PRJNA600494 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10869373.fastq.gz	Fastqsanger.gz
	SRR10869374.fastq.gz	Fastqsanger.gz
	SRR10869375.fastq.gz	Fastqsanger.gz
	SRR10869376.fastq.gz	Fastqsanger.gz
	SRR10869377.fastq.gz	Fastqsanger.gz

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GPER1 inhibits placental type I IFN responses to preserve fetal health during maternal infection

Project description:GPER1 inhibits placental type I IFN responses to preserve fetal health during maternal infection

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GPER1 inhibits placental type I IFN responses to preserve fetal health during maternal infection [GECKOscreen]

Project description:GPER1 inhibits placental type I IFN responses to preserve fetal health during maternal infection [GECKOscreen]

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GPER1 inhibits placental type I IFN responses to preserve fetal health during maternal infection [RNAseq]

Project description:Inhibition of GPER1 in pregnant mice significantly alters inflammation and angiogenesis in the placenta, but does not significantly impact the lung

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GPER1 inhibits placental type I IFN responses to preserve fetal health during maternal infection [GECKOscreen]

Project description:Identification of factors that control ifn responses during pregnancy

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GPER1 inhibits placental type I IFN responses to preserve fetal health during maternal infection

Project description:This SuperSeries is composed of the SubSeries listed below.

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Effects of maternal choline intake on placental gene expression

Project description:To explore the influence of maternal choline intake on placental gene expression, we employed whole genome microarray expression profiling to identify genes that were differentially expressed in placental tissues obtained from women consuming two different doses (480 vs. 930 mg/d) of choline throughout the third trimester of pregnancy. Healthy third trimester (gestational week 26-29) pregnant women were randomized to a 12-week choline controlled feeding study. The participants consumed either 480 (n=6) or 930 (n=6) mg choline/d. Full thickness placental samples were collected at delivery to extract RNA and perform the arrays. Healthy third trimester (gestational week 26-29) pregnant women were randomized to a 12-week choline controlled feeding study. The participants consumed either 480 (n=6) or 930 (n=6) mg choline/d for 12 weeks. Placental samples were obtained at delivery

2012-07-12 | E-GEOD-39290 | biostudies-arrayexpress

The maternal microbiome promotes placental development in mice

Project description:We report that depletion of the maternal microbiota results in abberant placental development in mice - these data show gene expression changes in E14.5 placental labyrinth samples from microbiota-depleted dams and controls.

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DNA hypermethylation in placental tissues: placental tissues vs. maternal peripheral bloods

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: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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IFN-kappa inhibits HPV31 transcription by inducing Sp100 proteins

Project description:Using doxycycline-inducible IFN-kappa expression in CIN612-9E cells, which maintain extrachromosomally replicating HPV31 genomes, we demonstrate that IFN-kappa inhibits the growth of these cells and reduces viral transcription and replication. Interestingly, the initiation of viral early transcription was already inhibited 4-6h after IFN-kappa expression. This was also observed with recombinant IFN-beta suggesting a common mechanism of IFNs. RNA-seq analysis identified 1367 IFN-kappa regulated genes of which 221 were modulated >2-fold. The majority of those (71%) matched known ISGs confirming that IFN-kappa acts as a bona fide type I IFN in hr-HPV-positive keratinocytes. RNAi and co-transfection experiments indicate that the inhibition of viral transcription is mainly due to the induction of Sp100 proteins by IFN-kappa. CIN612-9E/pInd-IFN-kappa were induced for 4h with 1Âµg/ml doxycyclin or not. Three biological replicates were analyzed.

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