Female- and male-specific transcriptomic and epigenetic placental signatures in response to a maternal high fat diet in mice
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE29585 | GEO | 2012/04/01
SECONDARY ACCESSION(S): PRJNA141421
REPOSITORIES: GEO
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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
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.
2021-03-12 | PXD023454 | Pride
Project description:Previously, we have examined the effect of maternal dietary n-3 LCPUFA supplementation during pregnancy to reduce offspring obesity risk. Considering the involvement of the placenta in fetal programming, we here analyzed the sexually dimorphic potential of placental gene expression, its response to the n-3 LCPUFA intervention and their correlation to offspring obesity risk. The placenta is implicated to play a key role in mediating fetal /metabolic programming of the offspring in utero. For human and mouse models, it has been reported that male and female fetuses differentially respond to in utero environmental stimuli. Moreover, sexual dimorphism is also known for placental gene expression, LCPUFA metabolism and adipose tissue distribution. Therefore, we explored whether the maternal n-3 LCPUFA intervention during pregnancy has a sex-specific impact on the term placental transcriptome in a defined subpopulation of the INFAT (impact of nutritional fatty acids during pregnancy and lactation on early human adipose tissue development) study. In addition, we assessed the relationships between sex-specific placental gene expression and sex steroids levels, and expression changes of specific genes and offspring obesity risk. Overall, human term placentas show sexually dimorphic gene expression and respond sex-specifically to dietary maternal n-3 LCPUFA intervention during pregnancy with more pronounced effects on gene expression and estradiol-17β/testosterone ratio in female than male placentas.
2014-10-30 | GSE53291 | GEO
Project description:The first trimester is a critical window of maternal-fetal communication for pregnancy. Using single cell RNA-sequencing to dissect placenta heterogeneity, we identified five major cell types (trophoblasts, stromal cells, hofbauer cells, antigen presenting cells and endothelial cells). We identified seven unique trophoblast subclusters, including new subtypes that transition into the terminal cell types, extra-villous trophoblasts and syncytiotrophoblasts. As fetal sex impacts pregnancy, we analyzed sex differences in each cell type and identified differences in immune cell function. TGFβ1, β-estradiol, and dihydrotestosterone emerge as upstream regulators of sexually dimorphic genes in a cell type specific manner. Thus, the fetal contribution at the maternal-fetal interface is cell and sex specific.
2020-08-20 | GSE131696 | GEO
Project description:As sex determines mammalian development, understanding the nature and developmental dynamics of the sexually dimorphic transcriptome is important. To explore this, we generated 72 genome-wide RNA-seq profiles from mouse eight-cell embryos, late gestation and adult livers, together with 4 ground-state pluripotent embryonic (ES) cell lines from which we generated both RNA-seq and multiple ChIP-seq profiles. We complemented this with previously published data to yield 5 snap-shots of pre-implantation development, late-gestation placenta and somatic tissue and multiple adult tissues for integrative analysis. We define a high-confidence sex-dimorphic signature of 56 genes in eight-cell embryos. Sex-chromosome-linked components of this signature are largely conserved throughout pre-implantation development and ES cells, whilst the autosomal component is more dynamic. Sex-biased gene expression is reflected by enrichment for activating and repressive histone modifications. The eight-cell signature is largely non-overlapping with that defined from fetal liver, neither was it correlated with liver or other adult tissues analysed. Fetal and adult liver gene expression signatures are also substantially different, yet a core set of common genes showing modest dimorphic expression was identified. Dramatic sex-specific expression of olfactory receptors was found in fetal liver. Sex-biased expression differences unique to adult liver were enriched for growth hormone-responsiveness. The majority of sex-chromosome based differences identified from eight-cell embryos are also present in placenta but not somatic tissue at the same gestational age. This systematic study identifies three distinct phases of sex dimorphism throughout mouse development, and has significant implications for understanding the developmental origins of sex-specific phenotypes and disease in mammals. ChIP seq of Es Cell
2015-05-26 | E-GEOD-59220 | biostudies-arrayexpress
Project description:As sex determines mammalian development, understanding the nature and developmental dynamics of the sexually dimorphic transcriptome is important. To explore this, we generated 72 genome-wide RNA-seq profiles from mouse eight-cell embryos, late gestation and adult livers, together with 4 ground-state pluripotent embryonic (ES) cell lines from which we generated both RNA-seq and multiple ChIP-seq profiles. We complemented this with previously published data to yield 5 snap-shots of pre-implantation development, late-gestation placenta and somatic tissue and multiple adult tissues for integrative analysis. We define a high-confidence sex-dimorphic signature of 56 genes in eight-cell embryos. Sex-chromosome-linked components of this signature are largely conserved throughout pre-implantation development and ES cells, whilst the autosomal component is more dynamic. Sex-biased gene expression is reflected by enrichment for activating and repressive histone modifications. The eight-cell signature is largely non-overlapping with that defined from fetal liver, neither was it correlated with liver or other adult tissues analysed. Fetal and adult liver gene expression signatures are also substantially different, yet a core set of common genes showing modest dimorphic expression was identified. Dramatic sex-specific expression of olfactory receptors was found in fetal liver. Sex-biased expression differences unique to adult liver were enriched for growth hormone-responsiveness. The majority of sex-chromosome based differences identified from eight-cell embryos are also present in placenta but not somatic tissue at the same gestational age. This systematic study identifies three distinct phases of sex dimorphism throughout mouse development, and has significant implications for understanding the developmental origins of sex-specific phenotypes and disease in mammals. Examination of the sexual dimorphisim during developmental stages of 8 Cell, Es Cell, Fetal Liver and Adult Liver
2015-05-26 | E-GEOD-58733 | biostudies-arrayexpress
Project description:The first trimester is a critical window of maternal-fetal communication for pregnancy. RNA-sequencing of matched maternal decidua (4) and placenta (4) identified 91 sexually dimorphic receptor-ligand pairs across the maternal-fetal interface, 32 in females and 59 in males.
2020-08-20 | GSE131874 | GEO
Project description:As sex determines mammalian development, understanding the nature and developmental dynamics of the sexually dimorphic transcriptome is important. To explore this, we generated 72 genome-wide RNA-seq profiles from mouse eight-cell embryos, late gestation and adult livers, together with 4 ground-state pluripotent embryonic (ES) cell lines from which we generated both RNA-seq and multiple ChIP-seq profiles. We complemented this with previously published data to yield 5 snap-shots of pre-implantation development, late-gestation placenta and somatic tissue and multiple adult tissues for integrative analysis. We define a high-confidence sex-dimorphic signature of 56 genes in eight-cell embryos. Sex-chromosome-linked components of this signature are largely conserved throughout pre-implantation development and ES cells, whilst the autosomal component is more dynamic. Sex-biased gene expression is reflected by enrichment for activating and repressive histone modifications. The eight-cell signature is largely non-overlapping with that defined from fetal liver, neither was it correlated with liver or other adult tissues analysed. Fetal and adult liver gene expression signatures are also substantially different, yet a core set of common genes showing modest dimorphic expression was identified. Dramatic sex-specific expression of olfactory receptors was found in fetal liver. Sex-biased expression differences unique to adult liver were enriched for growth hormone-responsiveness. The majority of sex-chromosome based differences identified from eight-cell embryos are also present in placenta but not somatic tissue at the same gestational age. This systematic study identifies three distinct phases of sex dimorphism throughout mouse development, and has significant implications for understanding the developmental origins of sex-specific phenotypes and disease in mammals.
2015-05-26 | GSE58733 | GEO
Project description:As sex determines mammalian development, understanding the nature and developmental dynamics of the sexually dimorphic transcriptome is important. To explore this, we generated 72 genome-wide RNA-seq profiles from mouse eight-cell embryos, late gestation and adult livers, together with 4 ground-state pluripotent embryonic (ES) cell lines from which we generated both RNA-seq and multiple ChIP-seq profiles. We complemented this with previously published data to yield 5 snap-shots of pre-implantation development, late-gestation placenta and somatic tissue and multiple adult tissues for integrative analysis. We define a high-confidence sex-dimorphic signature of 56 genes in eight-cell embryos. Sex-chromosome-linked components of this signature are largely conserved throughout pre-implantation development and ES cells, whilst the autosomal component is more dynamic. Sex-biased gene expression is reflected by enrichment for activating and repressive histone modifications. The eight-cell signature is largely non-overlapping with that defined from fetal liver, neither was it correlated with liver or other adult tissues analysed. Fetal and adult liver gene expression signatures are also substantially different, yet a core set of common genes showing modest dimorphic expression was identified. Dramatic sex-specific expression of olfactory receptors was found in fetal liver. Sex-biased expression differences unique to adult liver were enriched for growth hormone-responsiveness. The majority of sex-chromosome based differences identified from eight-cell embryos are also present in placenta but not somatic tissue at the same gestational age. This systematic study identifies three distinct phases of sex dimorphism throughout mouse development, and has significant implications for understanding the developmental origins of sex-specific phenotypes and disease in mammals.
2015-05-26 | GSE59220 | GEO
Project description:Ketogenic diet consumption elevates circulating levels of the ketones β-hydroxybutyrate (βOHB) and acetoacetate (AcAc). In vitro ketone exposure perturbs preimplantation mouse embryo viability and female-specific fetal development post-transfer. Here we assessed whether transient exposure of preimplantation embryos to ketones impacts post-implantation fetal and placental gene expression. Blastocysts cultured in vitro with or without 2 mmol/L βOHB alone (‘βOHB’) or combined with 0.8 mmol/L AcAc (‘Keto’) underwent embryo transfer. Transcriptional profiles of sexed E14.5 placentae, liver, and brain were examined via RNA-Seq and DAVID functional analysis, revealing a sexually dimorphic transcriptomic response. βOHB and Keto exposure both downregulated genes related to oxidative phosphorylation specifically in female liver. βOHB downregulated female placental steroid biosynthetic processes, while Keto treatment upregulated genes relevant to blood vessel formation and cell migration in male placentae. Brain transcriptomes were minimally affected. X-linked genes and chromatin modifiers were identified as differentially expressed, alluding to a sex-specific regulatory mechanism. Transient preimplantation ketone exposure therefore perturbs sex-specific fetal liver and placental gene expression demonstrating a developmental programming effect that warrants future investigation of male and female offspring postnatal metabolic health.
2023-09-15 | GSE217821 | GEO