Placenta-specific DMRs maintain methylation across gestation.
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ABSTRACT:
PROVIDER: PRJNA495474 | ENA |
REPOSITORIES: ENA
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Project description:One possible mechanism leading to the apparent polymorphic placenta-specific DMRs would be the failure to maintain allelic methylation during gestation. For a temporal comparison, we performed methylation profiling on first trimester chorionic villus sampling (CVS) and compared it with corresponding samples at term. This revealed that DNA methylation level at placenta-specific DMRs is highly stable between the two points. In addition, to ensure that the methylation profiles were uniform across the placental plate, we determined the placenta-specific DMR profiles from multiple biopsies from the same term placentas. Biopsies collected from the opposite sides of the cord insertion site also showed high correlations, suggesting that methylation does not vary greatly between sampling sites. Finally, we compared placenta samples from dizygotic twins and triplets. As in the other cases, this revealed that the correlations between samples of the same gestations (sharing the same in utero environment and maternal exposures) were also higher than between unrelated samples.
2019-02-05 | GSE121056 | GEO
Project description:Background: The placenta is vital for fetal development and its contributions to various developmental issues, such as pregnancy complications, fetal growth restriction, and maternal exposure, have been extensively studied in mice. Contrary to popular belief, the placenta forms mainly from fetal tissue; therefore, it has the same biological sex as the fetus it supports. However, while placental function is linked to increased risks of pregnancy complications and neurodevelopmental diseases in male offspring in particular, the sex-specific epigenetic (e.g., DNA methylation) and transcriptomic features of the late-gestation mouse placenta remain largely unknown.Methods: We collected male and female mouse placentas at late gestation (E18.5, n = 3/sex) and performed next-generation sequencing to identify genome-wide sex-specific differences in transcription and DNA methylation. Results: Our sex-specific analysis revealed 358 differentially expressed genes (DEGs) on autosomes, which were associated with signaling pathways involved in transmembrane transport and the responses to viruses and external stimuli. X chromosome DEGs (n = 39) were associated with different pathways, including those regulating chromatin modification and small GTPase-mediated signal transduction. Sex-specific differentially methylated regions (DMRs) were more common on the X chromosomes (n = 3756) than on autosomes (n = 1705). Interestingly, while most X chromosome DMRs had higher DNA methylation levels in female placentas and tended to be included in CpG dinucleotide-rich regions, 73% of autosomal DMRs had higher methylation levels in male placentas and were distant from CpG-rich regions. Several sex-specific DEGs were correlated with sex-specific DMRs. A subset of the sex-specific DMRs present in late-stage placentas were already established in mid-gestation (E10.5) placentas, while others were acquired later in placental development.Conclusion: Our study provides comprehensive lists of sex-specific DEGs and DMRs that collectively cause profound differences in the DNA methylation and gene expression profiles of late-gestation mouse placentas. Our results demonstrate the importance of incorporating sex-specific analyses into epigenetic and transcription studies to enhance the accuracy and comprehensiveness of their conclusions and help address the significant knowledge gap regarding how sex differences influence placental function.
2023-12-30 | GSE252283 | GEO
Project description:Background: The placenta is vital for fetal development and its contributions to various developmental issues, such as pregnancy complications, fetal growth restriction, and maternal exposure, have been extensively studied in mice. Contrary to popular belief, the placenta forms mainly from fetal tissue; therefore, it has the same biological sex as the fetus it supports. However, while placental function is linked to increased risks of pregnancy complications and neurodevelopmental diseases in male offspring in particular, the sex-specific epigenetic (e.g., DNA methylation) and transcriptomic features of the late-gestation mouse placenta remain largely unknown.Methods: We collected male and female mouse placentas at late gestation (E18.5, n = 3/sex) and performed next-generation sequencing to identify genome-wide sex-specific differences in transcription and DNA methylation. Results: Our sex-specific analysis revealed 358 differentially expressed genes (DEGs) on autosomes, which were associated with signaling pathways involved in transmembrane transport and the responses to viruses and external stimuli. X chromosome DEGs (n = 39) were associated with different pathways, including those regulating chromatin modification and small GTPase-mediated signal transduction. Sex-specific differentially methylated regions (DMRs) were more common on the X chromosomes (n = 3756) than on autosomes (n = 1705). Interestingly, while most X chromosome DMRs had higher DNA methylation levels in female placentas and tended to be included in CpG dinucleotide-rich regions, 73% of autosomal DMRs had higher methylation levels in male placentas and were distant from CpG-rich regions. Several sex-specific DEGs were correlated with sex-specific DMRs. A subset of the sex-specific DMRs present in late-stage placentas were already established in mid-gestation (E10.5) placentas, while others were acquired later in placental development.Conclusion: Our study provides comprehensive lists of sex-specific DEGs and DMRs that collectively cause profound differences in the DNA methylation and gene expression profiles of late-gestation mouse placentas. Our results demonstrate the importance of incorporating sex-specific analyses into epigenetic and transcription studies to enhance the accuracy and comprehensiveness of their conclusions and help address the significant knowledge gap regarding how sex differences influence placental function.
2023-12-30 | GSE252281 | GEO
Project description:Background : The placenta is vital for fetal development and its contributions to various developmental issues, such as pregnancy complications, fetal growth restriction, and maternal exposure, have been extensively studied in mice. The placenta forms mainly from fetal tissue and therefore has the same biological sex as the fetus it supports. Extensive research has delved into the placenta’s involvement in pregnancy complications and future offspring development, with a notable emphasis on exploring sex-specific disparities. However, despite these investigations, sex-based disparities in epigenetic (e.g., DNA methylation) and transcriptomic features of the late-gestation mouse placenta remain largely unknown. Methods : We collected male and female mouse placentas at late gestation (E18.5, n = 3/sex) and performed next-generation sequencing to identify genome-wide sex differences in transcription and DNA methylation. Results Our comparison between male and female revealed 358 differentially expressed genes (DEGs) on autosomes, which were associated with signaling pathways involved in transmembrane transport and the responses to viruses and external stimuli. X chromosome DEGs (n = 39) were associated with different pathways, including those regulating chromatin modification and small GTPase-mediated signal transduction. Differentially methylated regions (DMRs) were more common on the X chromosomes (n = 3756) than on autosomes (n = 1705). Interestingly, while most X chromosome DMRs had higher DNA methylation levels in female placentas and tended to be included in CpG dinucleotide-rich regions, 73% of autosomal DMRs had higher methylation levels in male placentas and were distant from CpG-rich regions. Several DEGs were correlated with DMRs. A subset of the DMRs present in late-stage placentas were already established in mid-gestation (E10.5) placentas (n = 348 DMRs on X chromosome and 19 DMRs on autosomes), while others were acquired later in placental development. Conclusion : Our study provides comprehensive lists of DEGs and DMRs between male and female that collectively cause profound differences in the DNA methylation and gene expression profiles of late-gestation mouse placentas. Our results demonstrate the importance of incorporating sex-specific analyses into epigenetic and transcription studies to enhance the accuracy and comprehensiveness of their conclusions and help address the significant knowledge gap regarding how sex differences influence placental function.
2023-12-31 | GSE252282 | GEO
Project description:The goal of this study was to transciprtionally profile the three layers of the human placenta (decidua, fetal membrane and placental villi) from the mid-gestation healthy human placenta.
2022-01-27 | GSE178152 | GEO
Project description:In early embryos, DNA methylation is remodelled to initiate the developmental program. For mostly unknown reasons, methylation marks are acquired unequally between embryonic and placental cells. To better understand this, we generated high-resolution maps of DNA methylation in mouse mid-gestation (E10.5) embryo and placenta. We uncovered specific subtypes of differentially methylated regions (DMRs) that contribute directly to the developmental asymmetry existing between mid-gestation embryo and placenta. We show that the asymmetry between embryonic and placental DNA methylation patterns occurs rapidly during the acquisition of marks in the post-implanted conceptus (E3.5-E6.5), and that these patterns are long-lasting across subtypes of DMRs throughout prenatal development and in somatic tissues. We reveal that at the peri-implantation stages, the de novo methyltransferase activity of DNMT3B is the main driver of methylation marks on asymmetric DMRs, and that DNMT3B can largely compensate for lack of DNMT3A in the epiblast and extraembryonic ectoderm, whereas DNMT3A can only partially palliate for the absence of DNMT3B. However, as development progresses and as DNMT3A becomes the principal de novo methyltransferase, the compensatory DNA methylation mechanism on DMRs becomes less effective.
2020-02-18 | GSE95610 | GEO
Project description:The placenta has a critical role in fetal growth, with many key functions regulated by genomic imprinting. With the recent description of polymorphic placenta-specific imprinting, the molecular mechanisms leading to this curious epigenetic phenomenon are unknown, as is their involvement in pregnancies complications. Profiling ubiquitous and placenta-specific imprinted differentially methylated regions (DMRs) exposed isolated aberrant methylation at ubiquitous DMRs as well as abundant hypomethylation at placenta-specific DMRs. Analysis of underlying chromatin at polymorphic placenta-specific imprinted DMRs revealed biallelic enrichment of histone H3K4 methylation, a modification normally mutually exclusive with DNA methylation. Furthermore, characterisation of expression in intrauterine growth restricted samples (IUGRs) uncovered coordinated deregulation of the GPR1AS1-ZDBF2-ADAM23 locus. Our results emphasize that methylation is less stable at placenta-specific imprints compared to their ubiquitous counterparts and that further work is required to determine if these differences are the IUGR cause or reflect unique adaption of the placenta epigenome to developmental stresses.
2019-02-05 | GSE120981 | GEO
Project description:Gene Expression of mid-gestation human placenta
| PRJNA737475 | ENA
Project description:We report the RNAseq-based mRNA and microRNA transcriptome profiles of gestation day 21 female rat liver and placenta following oral ketoconazole exposure from gestation day 6 to 20. A treatment-related change in mRNA and microRNA levels was observed in both liver and placenta.
2022-05-02 | GSE200184 | GEO
Project description:Examined the role of maternal voluntary wheel running commencing 10 weeks prior to gestation, and throughout pregnancy, on placental transcriptome in late gestation While exercise (EX) is beneficial during pregnancy for both mother and child, little is known about the mechanisms by which maternal (MAT EX) mediates changes in utero. We hypothesized that effects of MAT EX prior to and during gestation will be evident in transcriptomic signatures in the placenta and will be sexually dimorphic. Six-week-old female C57BL/6 mice were divided into 2 groups; with (exercise, EX; N = 7) or without (sedentary, SED; N = 8) access to voluntary running wheels. EX was provided via 24-hour access to wheels for 10 weeks prior to conception until late pregnancy (18.5 days post coitum). Sex-stratified placenta and fetal livers were collected. Mi-croarray analysis of SED and EX placenta revealed that MAT EX affected gene transcript expression of 283 and 661 transcripts in male and female placenta (±1.4-fold, p < 0.05). Gene-set enrichment and Ingenuity Pathway analyses of male placenta showed that MAT EX led to inhibition of sig-naling pathways, biological functions, and down regulation of transcripts related to lipid and steroid, while MAT EX in female placentas led to activation of pathways, biological functions, and gene expression related to muscle growth, brain, vascular development, and growth factors. Overall, our results suggest that effects of MAT EX on the placenta and presumably on the offspring are influenced by maternal habitus and are sexually dimorphic.
2024-01-31 | GSE243228 | GEO