Effect of maternal iron deficiency on placental gene expression on gestational day 18.5 in rats
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA685357 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Iron deficiency occurs when iron demands chronically exceed intake, and is particularly prevalent in pregnant women. Iron deficiency during pregnancy poses health risks for the baby. The placenta serves as the interface between a pregnant mother and her baby; thus, maternal iron deficiency may indirectly impact fetal growth and development by altering placental function. In this study, pregnant Sprague-Dawley rats were fed either a low-iron or iron-replete diet starting two weeks before mating. On gestational day 18.5, RNA was collected, and a Clariom S microarray was performed to elucidate differences in gene expression between gestaional day 18.5 placentas isolated from dams fed iron replete or iron deficient diets.
2021-11-10 | GSE163226 | GEO
Project description:Zinc is an essential micronutrient in pregnancy and zinc deficiency impairs fetal growth. We used a mouse model of moderate zinc deficiency to determine how zinc is important to placental morphogenesis. Global placental gene expression at gestational day 18.5 was analysed using microarray to determine the effects of zinc deficiency on placental function.
2018-02-13 | GSE97112 | GEO
Project description:the goal of this study is to use high-throughput RNA-Sequencing technology to identify genes that are differentially expressed in iron deficient (ID) placentas compared to iron adequate (IA) placentas. A secondary aim is to explore whether iron deficiency has differential impact on male compared with female placental transcriptome.
2020-09-23 | GSE157667 | GEO
Project description:To investigate the effects of gestational exposure to ozone, we performed single-cell RNA-sequencing on murine placental tissues.
2024-06-30 | GSE234021 | GEO
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: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
Project description:A physiological state of insulin resistance is required to preferentially direct maternal nutrients toward the feto-placental unit, allowing adequate growth of the fetus. When women develop gestational diabetes mellitus (GDM), insulin resistance is more severe and disrupts the intrauterine milieu, resulting in accelerated fetal development with increased risk of macrosomia. As a natural interface between mother and fetus, the placenta is the obligatory target of such environmental changes. However, the molecular basis for the imbalance that leads to fetal, neonatal, and adult metabolic compromises is not well understood. We report that GDM elicits major changes in the expression profile of placental genes with a prominent increase in markers and mediators of inflammation. Within the 435 transcripts reproducibly modified, genes for stress-activated and inflammatory responses represented the largest functional cluster (18.5% of regulated genes). Upregulation of interleukins, leptin, and tumor necrosis factor-{alpha} receptors and their downstream molecular adaptors indicated an activation of pathways recruiting stress-activated protein/c-Jun NH2-terminal kinases. Transcriptional activation of extracellular matrix components and angiogenic activators pointed to a major structural reorganization of the placenta. Thus, placental transcriptome emerges as a primary target of the altered environment of diabetic pregnancy. The genes identified provide the basis to elucidate links between inflammatory pathways and GDM-associated insulin resistance. Keywords: other
2005-07-18 | GSE2956 | GEO
Project description:We report the expression pattern of placental transcriptome by Next Generation Sequencing from Gestational D19 mouse exposed to Air -Pollutant material with or without prior treatment with Fish Oil.
2022-05-25 | GSE178098 | GEO
Project description:Intrauterine growth restriction (IUGR) affects up to 10% of pregnancies and often results in short- and long- term sequelae for offspring, including risk for adult cardiovascular disease (CVD). The mechanisms underlying IUGR are poorly understood, though poor blood flow and oxygen/nutrient provision to the IUGR fetus are thought to be the common endpoints of disease. Though several animal models of IUGR exist, few demonstrate later phenotypes of CVD despite a large body of evidence in humans linking IUGR and adult CVD onset. We thus hypothesized that in murine pregnancy, maternal late gestational hypoxia (LG-H) exposure resulting in IUGR would result in (1) adult phenotypes of CVD in hypoxia-exposed offspring, and (2) the placental transcriptome will demonstrate alterations that can be linked to risk of later disease. After subjecting pregnant mice to hypoxia (10.5% oxygen) from gestational day (GD) 14.5 to 18.5, we collected placentas at GD19. We examined RNA isolated from these placentas to perform RNA sequencing and analysis. Functional gene and cluster-based analysis suggest multiple changes in structural and functional genes important for placental health, with the top dysregulation involving vascular and metabolic pathways. Concordantly, a ~ 10% decrease in birthweights and ~30% decrease in litter size after LG-H (p<0.05) was observed, suggesting an environment of placental insufficiency. We also found that offspring exposed in-utero to LG-H exhibit CVD at 4 months of age, with males being worse than females, supporting developmental programming. Specifically, males exhibit increased body weight and an enlarged heart size, whereas both males and females develop hypertension, elevated abdominal fat, elevated leptin and elevated total cholesterol levels with aging. In summary, LG-H exposure in the pregnant mouse mimics human placental insufficiency related IUGR. The placentas of these exposed fetuses demonstrate a transcriptional response to the stressor of gestational hypoxia and predicts cardiovascular and metabolic effects that culminate into hypertension and adiposity with dyslipidemia.
2019-02-13 | GSE112755 | GEO
Project description:Tissue specific DNA methylation is present across many genomic elements, including large genomic regions. Most human tissues posses highly methylated genomes (>70%), but recent data has suggested the presence of partially methylated domains (PMDs) in some cell-lines. Placenta is a unique human tissue which has very different molecular properties than most tissues. It is the aim of this study to identify the presence/absence of PMDs in placental tissue and further define the DNA methylation landscape of the placenta. In particular this experiment is designed to look at the placental methylome across gestational ages in chromosome 21 to detect methylomic differences throughout development.
2013-03-29 | E-MTAB-1508 | biostudies-arrayexpress