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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Effect of NDRG1 deletion and hypoxia in mouse placenta

ABSTRACT: We sought to identify changes in placental gene expression that may contribute to the phenotype of NDRG1-deficient embryos, and to define the contribution of hypoxia and fetal sex to these changes. We therefore used high-density oligonucleotide microarrays to interrogate differences in placental gene expression, stratified by fetal sex, Ndrg1 status (WT vs KO) and oxygenation (21% vs 12%). C57Bl6/J mice heterozygous for NDRG1-null allele were bred and separated next day (E0.5), and give ad libitum access to standard chow and water with 12h light:dark cycle. Pregnant dams were sacrificed at E15.5 by cervical dislocation following isoflurane anesthesia. Following sacrifice, embryos and placentas were collected, NDRG1 genotype and sex were determined by PCR of fetal tissue, and RNA was extracted from placental tissue following removal of membranes.

ORGANISM(S): Mus musculus

SUBMITTER: Jacob Larkin

PROVIDER: E-GEOD-46381 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Effect of NDRG1 deletion and hypoxia in mouse placenta

Project description:We sought to identify changes in placental gene expression that may contribute to the phenotype of NDRG1-deficient embryos, and to define the contribution of hypoxia and fetal sex to these changes. We therefore used high-density oligonucleotide microarrays to interrogate differences in placental gene expression, stratified by fetal sex, Ndrg1 status (WT vs KO) and oxygenation (21% vs 12%).

2013-04-26 | GSE46381 | GEO

Female- and male-specific transcriptomic and epigenetic placental signatures in response to a maternal high fat diet in mice

Project description:Overnutrition during pregnancy inM-oM-,M-^Buences the future health of the offspring, with outcomes differing depending on the childM-bM-^@M-^Ys sex. The placenta is involved in the programming of obesity, type 2 diabetes and cardiovascular disease. Sex-specific adaptation of the placenta may be central to the differences in fetal growth and survival. The impact of diet and fetal sex on placental gene expression and epigenetic marks was investigated in mice fed a high-fat (HFD) or a control diet (CD), during the first 15 days of gestation Microarrays analysis revealed that expression was affected by maternal diet and was sexually dimorphic. We analyzed the placentae of 4 mice litters fed with an high-fat diet (HFD) and 4 with a control diet (CD). For each litter, the placenta transcriptome was analysed according to the foetus sex using the Affymetrix Human Exon 1.0 ST platform. Array data was processed by Affymetrix Exon Array Computational Tool. No technical replicates were performed.

2012-03-31 | E-GEOD-29585 | biostudies-arrayexpress

Exposure to lipopolysaccharide induces sexually dimorphic placental adaptation by modifying placental efficiency, morphogenesis, and gene expression

Project description:Sexual dimorphism in placental physiology during development affects the functionality of placental adaptation during adverse pregnancy, affecting fetal growth, development, and eventually fetal programming, which have long-term effects on the offspring’s adult life. However, studies focusing on the phenomenon and relationship between sex-specific placental adaptation and consequent altered fetal development are still elusive. Here, we established a prenatal maternal stress model by administering lipopolysaccharide (LPS) to pregnant ICR mice at the mid-gestational stage. To verify the appropriateness of the animal model to study sex differences in the sub-optimal uterus milieu, pregnancy complications were examined. To elucidate global transcriptomic changes occurring in the placenta, total RNA sequencing was performed in female and male placentas. LPS exposure at the mid-gestational stage induced placental inflammation in both sexes. In utero inflammatory conditions resulted in intrauterine fetal growth restriction and impaired placental development in a sex-specific manner depending on the dose of LPS. Sex-biased placental pathology was observed in the junctional zone and the labyrinth layer. Placental transcriptome analysis revealed widespread disparity in protein-coding and long non-coding genes between female and male placentas, presenting the relationship between morphology and function in a sex-specific IUGR model.

2021-08-26 | GSE182462 | GEO

Placental gene expression in intestinal nematode-infected and protein-deficient mice

Project description:Protein deficiency and intestinal parasite infection during pregnancy impair fetal growth through passage of signals from the maternal environment which signal impairment of fetal growth. The placenta is an important regulator of the transfer of these signals through differential expression of key placental genes. We used microarrays to examine placental gene expression responses to maternal protein deficiency (6% vs. 24% protein) and Heligmosomoides bakeri infection. 2x2 factorial.

2015-09-09 | E-GEOD-57115 | biostudies-arrayexpress

Gene expression variation in horse placental and fetal tissue, and resting and stimulated horse lymphocytes

Project description:This SuperSeries is composed of the following subset Series: GSE35741: Gene expression variation in horse placental and fetal tissue, and resting and stimulated horse lymphocytes [Agilent-018932] GSE35742: Gene expression variation in horse placental tissue, and resting and stimulated horse lymphocytes [Agilent-021322] Refer to individual Series

2012-02-14 | E-GEOD-35743 | biostudies-arrayexpress

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

The human placental sexome differs between trophoblast epithelium and villous vessel endothelium

Project description:As susceptibility to many adult disorders originates in utero, we here hypothesized that fetal sex influences gene expression in placental cells and produces functional differences in human placentas. We found that fetal sex differentially affects gene expression in a cell-phenotype dependent manner among all four placental cell-phenotypes studied: cytotrophoblasts, syncytiotrophoblasts, arterial endothelial cells and venous endothelial cells. The markedly enriched pathways in males were identified to be signaling pathways for graft-versus-host disease as well as the immune and inflammatory systems, both supporting the hypothesis that there is reduced maternal-fetal compatibility for male fetuses. Our study is the first microarray study investigating sexual dimorphism in purified and characterized somatic cells from a single human tissue, the placenta, that underlines the importance of considering fetal sex as an independent variable in any work using human placenta.

2013-10-01 | GSE44368 | GEO

Expression of the placental transcriptome in fetal growth restriction in the Baboon is Dependent on Fetal Sex

Project description:Fetal growth restriction (FGR) develops when fetal nutrient availability is compromised and increases the risk for perinatal complications and predisposes for offspring obesity, diabetes and cardiovascular disease later in life. Emerging evidence implicates changes in placental function in altered fetal growth and the subsequent development of adult disease. The susceptibility for disease in response to an adverse intrauterine environment differs distinctly between boys and girls, with girls typically having better outcomes. Here, we test the hypothesis that regulation of the placental transcriptome by moderate nutrient reduction is dependent on fetal sex. We used a non-human primate model of FGR in which maternal global food intake is reduced by 30% starting at gestational day (GD) 30. At GD 165 (term = GD 183) placental genome expression profiling was carried out followed by bioinformatics including pathway and network analysis. Surprisingly, there was no coordinated placental molecular response to decreased nutrient availability when analyzing the data without accounting for fetal sex. In contrast, female placentas exhibited a highly coordinated response that included up-regulation of genes in networks, pathways and functional groups related to programmed cell death and down-regulation of genes in networks, pathways and functional groups associated with cell proliferation. These changes were not apparent in the male placentas. Our data support the concept that female placentas initiate complex adaptive responses to an adverse intrauterine environment, which may contribute to increased survival and better pregnancy outcomes in girls. Total RNA obtained from 165dGA control female (n=3), control male (n=3), nutrient restricted female (n=3), and nutrient restricted male (n=3) pregnancies.

2013-12-06 | E-GEOD-40878 | biostudies-arrayexpress

Pre-eclampsia TAC-seq

Project description:The etiology of preeclampsia, a hypertensive disorder of human pregnancy, remains unknown. We addressed fetal sex selection and the suggestive role of fetal HLA-G and related genes, regulating maternal immune responses, in preeclampsia pathogenesis. We assessed birth sex ratios, weights, and seasonality of preeclampsia among 1.79 million births in Finland. We studied haplotypes of HLA-G 3’ untranslated region (UTR), regulating HLA-G expression, in 1000 Genomes series and in a preeclampsia cohort (n=1249). We quantified placental (n=163) mRNA expression of 136 genes, studied HLA-G and IFNα protein expression by immunohistochemistry, and measured maternal and fetal circulating IFNα levels by ELISA. Population-level data showed loss of male fetuses as a characteristic of preeclampsia. As a potential contributor to immune-mediated loss, we found balancing selection at HLA-G 3’UTR modulating sex ratio, and association of HLA-G 3’UTR haplotypes with placental HLA-G expression. HLA-G and its receptors were downregulated in preeclampsia placentas, and surprisingly, interferon alpha-1 (IFNA1) was highly upregulated. IFNA1 and HLA-G distinguished preeclampsia better than placental FLT1 expression. Fetal but not maternal circulating IFNα, produced by trophoblasts, showed association with maternal hypertension and fetal growth restriction. We uncover the link between placental HLA-G expression and human birth sex ratio. We propose that preeclampsia shares, through reduced HLA-G mediated immunotolerance, the mechanism needed to fight placental viral infections and malaria in evolution. IFNα upregulation in preeclampsia placenta, together with its known actions upstream of inflammatory genes, encourages testing IFNα inhibitors and especially the pregnancy-approved antimalarial hydroxichloroquine in treatment of preeclampsia.

2019-11-25 | GSE125460 | 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

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