Fetal liver programming induced by placental endocrine malfunction
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB51067 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR8701690.fastq.gz | Fastqsanger.gz | |||
| ERR8701700.fastq.gz | Fastqsanger.gz | |||
| ERR8701691.fastq.gz | Fastqsanger.gz | |||
| ERR8701701.fastq.gz | Fastqsanger.gz | |||
| ERR8701692.fastq.gz | Fastqsanger.gz |
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Project description:The placenta acts as an interface between the mother and fetus, regulating nutrient transport and secreting hormones which impact maternal metabolism. Complications during pregnancy, such as placental endocrine malfunction, programme offspring to develop metabolic disease during adulthood, in part via changes in gene expression in critical metabolic organs, such as the liver, during fetal development. Placental endocrine malfunction was induced via the misexpression of two imprinted genes (Igf2 and H19) exclusively in the endocrine zone of the mouse placenta, to study the consequences this has on fetal hepatic gene expression.
2023-11-30 | E-MTAB-11457 | biostudies-arrayexpress
Project description:The placenta is a potent endocrine organ that secretes hormones with metabolic effects into maternal circulation. On the other hand, the liver, which is the main detoxification organ of the body, plays a key role in regulating maternal glucose and insulin metabolism during pregnancy. Failures in the production of placental hormones and/or the liver to adapt its structure and function to pregnancy can result in metabolic diseases such as gestational diabetes. Previous work has shown that the imprinted Igf2-H19 locus is involved in controlling placental endocrine function in mice. This study used conditional mis-expression of the Igf2-H19 locus to induce placental endocrine malfunction and study its consequences on hepatic gene regulation during pregnancy.
2024-11-27 | E-MTAB-11439 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the following subset Series: GSE33737: Fetal programming of muscle transcriptome in response to gestational dietary protein levels in the pig [AP] GSE33738: Fetal programming of muscle transcriptome in response to gestational dietary protein levels in the pig [HP] GSE33739: Fetal programming of muscle transcriptome in response to gestational dietary protein levels in the pig [LP] Refer to individual Series
2012-09-05 | E-GEOD-33740 | biostudies-arrayexpress
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
Project description:Intra-uterine growth restriction (IUGR) and fetal overgrowth increase the risk of postnatal health. Maternal nutrition is the major intrauterine environmental factor that alters fetal weight. However, the mechanisms underlying maternal nutrition affect fetal development is not entirely clear. We developed a pig model and used isobaric tags for relative and absolute quantification (iTRAQ) to investigate alterations in the placental proteome were obtained from gilts in normal-energy-intake (Con) and high-energy-intake (HE) group, respectively.At 90 d of gestation, the heavy fetuses were found at the tubal ends and light fetuses at the cervical ends of the uterus in Con group and the heavy fetuses had higher glucose concentration than the light fetuses. However, a higher uniformity was noted in HE group. Placental promote between these two positions indicated that a total of 78 and 50 differentially expressed proteins were detected in Con and HE group, respectively. In Con group, these proteins related to lipid metabolism (HADHA, AACS, CAD), nutrient transport (GLUT, SLC27A1) and energy metabolism (NDUFV1, NDUFV2, ATP5C1). However, the differentially expressed proteins in HE group were mainly participation in transcriptional and translational regulation and intracellular vesicular transport.
2018-10-26 | PXD004951 | Pride
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
Project description:This SuperSeries is composed of the following subset Series: GSE25482: Fetal programming of hepatic transcriptome in response to gestational dietary protein levels in the pig (AP data set) GSE25483: Fetal programming of hepatic transcriptome in response to gestational dietary protein levels in the pig (HP data set) Refer to individual Series
2011-11-30 | E-GEOD-25484 | biostudies-arrayexpress
Project description:Purpose: Identify differences in gene expression profiles in fetal monocytes - cells that persist and differentiate postnatally - according to distinct placental histologic domains. Methods: We first isolated classical and intermediate monocyte subsets via FACS and performed transcriptomic profiling of 140 samples (70 classical and 70 intermediate monocyte samples) using bulk RNA-Seq. Results: We report that placental lesions are associated with gene expression changes in fetal monocyte subsets. Specifically,fetal monocytes exposed to acute placental inflammation upregulate biological processes related to monocyte activation, monocyte chemotaxis, and platelet function while monocytes exposed to maternal vascular malperfusion lesions downregulate these processes. Additionally, we show that intermediate monocytes might be a source of mitogens, such as HBEGF, NRG1, and VEGFA, implicated in different outcomes related to prematurity. Conclusions: This is the first study to show that placental lesions are associated with unique changes in fetal monocytes and monocyte subsets. As fetal monocytes persist and differentiate into various phagocytic cells following birth, our study may provide insight into morbidity related to prematurity and ultimately potential therapeutic targets.
2022-02-02 | GSE195727 | GEO
Project description:Myostatin (gene symbol: <i>Mstn</i>) is an autocrine and paracrine inhibitor of muscle growth. Pregnant mice with genetically reduced levels of myostatin give birth to offspring with greater adult muscle mass and bone biomechanical strength. However, maternal myostatin is not detectable in fetal circulations. Fetal growth is dependent on the maternal environment, and the provisioning of nutrients and growth factors by the placenta. Thus, this study examined the effect of reduced maternal myostatin on maternal and fetal serum metabolomes, as well as the placental metabolome. Fetal and maternal serum metabolomes were highly distinct, which is consistent with the role of the placenta in creating a specific fetal nutrient environment. There was no effect from myostatin on maternal glucose tolerance or fasting insulin. In comparisons between pregnant control and <i>Mstn</i><sup>+/-</sup> mice, there were more significantly different metabolite concentrations in fetal serum, at 50, than in the mother's serum at 33, confirming the effect of maternal myostatin reduction on the fetal metabolic milieu. Polyamines, lysophospholipids, fatty acid oxidation, and vitamin C, in fetal serum, were all affected by maternal myostatin reduction.
2023-06-08 | MTBLS3345 | MetaboLights
Project description:This study aims to identify genome-wide placental DNA differential methylation positions (DMPs) in fetal overgrowth and the associations with fetal growth factors, leptin and adiponectin. In the Shanghai Birth Cohort, we studied 30 pairs of placentals of large-for-gestational-age (LGA, birth weight>90th percentile, an indicator of fetal overgrowth) and optimal-for-gestational-age (OGA, 25th-75th percentiles, control) newborns matched by sex and gestational age. Placental DNA methylations were measured by the Illumina Infinium Human Methylation-EPIC BeadChip. Cord blood insulin, C-peptide, proinsulin, IGF-1, IGF-2, leptin and adiponectin concentrations were measured. We identified 543 DMPs (397 hypermethylated, 146 hypomethylated) comparing LGA vs. OGA at false discovery rate <5% and absolute methylation difference >0.05 adjusting for placental cell type heterogeneity, maternal age, pre-pregnancy BMI and HbA1c levels during pregnancy. We validated a hyper-methylated gene - cadherin 13 (CDH13) reported in a previous epigenome-wide association study, and validated a newly discovered differentially (hyper-)methylated gene -visual system homeobox 1 (VSX1) in an independent pyrosequencing study sample (47 LGA-control pairs). Pathway analysis did not detect any statistically significant pathway correcting for multiple tests. Adiponectin in cord blood was correlated with its gene methylation in the placenta, while other observed biomarkers were not. Fetal overgrowth was associated with a large number of altered placental gene DNA methylations. The study provides robust evidence suggesting that placental CDH13 and VSX1 genes are hyper-methylated in LGA. Placental gene methylation was correlated with cord blood biomarker for adiponectin, but not for leptin and fetal growth factors.
2022-12-31 | GSE204977 | GEO