Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1005332 | ENA |
REPOSITORIES: ENA
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Project description:Methylation profiling of CpG Island Methylation of genomic DNA samples extracted from placentae of Intra-Uterine Growth Restricted newborns and gestational age matched controls. These data can be used for methylation comparisons between these two types of samples. The results of such comparisons can be used to generate hypotheses on the involvement of DNA methylation variation in placenta development and fetal growth. Two-condition Methyl DNA Immunoprecipitation (MeDIP) experiment, IUGR vs. Control placenta samples. Biological replicates: 8 control, 8 IUGR cases.
2011-04-11 | E-GEOD-22326 | biostudies-arrayexpress
Project description:Fetal growth in utero is affected by both inherent genetic programming in combination with environmental factors, such as maternal health and nutrition. Epidemiologic data in growth-altered fetuses, either growth-restricted (IUGR) or large for gestational age (LGA), demonstrate compelling evidence that these fetuses are at increased risk for cardiovascular and metabolic disease in adulthood. In this study, we used RRBS to examine genome wide DNA methylation variation in placental samples from offspring born IUGR, LGA, and appropriate for gestational age (AGA). We identified almost 200 differentially methylated genes among these groups. Among these genes, the differentially methylated regions were disproportionately located in transcription-regulatory regions such as promoters. Our results suggest that the gene expression and methylation state of the human placenta are related and sensitive to the intrauterine environment. We profiled DNA methylation for 17 human placentas, in which 5 were from LGA, 6 from IUGR and 6 from AGA placentas as controls
2015-06-30 | E-GEOD-70364 | biostudies-arrayexpress
Project description:Intrauterine growth restriction (IUGR) represents a major obstetric challenge with perinatal complications and a risk factor of developing disease in adult life. Placental insufficiency is one of the common features accompanying IUGR. The aim of this study was to evaluate global placental gene expression profile in IUGR compared to normal pregnancies. Placental samples were collected by eight IUGR pregnancies with placental insufficiency ascertained by Doppler and eight healthy controls. A 30K Human Genome Survey Microarray v.2.0 (Applied Biosystems) was used to evaluate global gene expression profile. Principal component analysis showed good separation in terms of gene expression patterns between the groups. Pathway analysis with Bonferroni correction for multiple testing showed significant (p<0.05) up-regulation of inflammation mediated by chemokine and cytokine signalling pathway in the IUGR placentas. Genes involved in metabolism of glucocorticoids (HSD11B1 and DHRS2) were found differentially expressed. We found no imprinted genes to be differentially expressed and only one gene involved in epigenetic modifications (MBD3) to be down-regulated in the IUGR placentas, indicating that IUGR due to placental insufficiency is not associated to placental imprinting. Subgroup analysis between pure IUGR and IUGR with preeclampsia placentas showed only 27 differentially expressed genes suggesting common pathophysiology. Eight placental samples from normal human placenta compared to eight human placental samples from patients with intrauterine growth restrictions due to placental insufficiency
2008-08-01 | E-GEOD-12216 | biostudies-arrayexpress
Project description:gut microbiota of IUGR pig Metagenome
| PRJNA1067849 | ENA
Project description:Placenta transcriptome profiling in Intrauterine Growth Restriction (IUGR)
| PRJEB30656 | ENA
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:The placental microvasculature of the human fetus is essential for the efficient transfer of gases, nutrients and waste between the mother and fetus. Microvascular hypoplasia of the terminal villi is associated with the placental pathology observed in cases of severe Intra Uterine Growth Restriction (IUGR). We used novel methods to isolate a pure population of placental microvascular endothelial cells from control preterm placentas (n=3) and placenta complicated by severe IUGR (n=6) with superimposed preeclampsia (n=5). Distal placental villous tissue was collected to enrich for terminal villi. Tissue was minced, digested and placental microvascular endothelial cells (PlMEC) were positively selected using tocosylated magnetic Dynabeads labeled with Human Endothelial Antigen lectin. The purity of the PlMEC (95%) was assessed by CD31 immunocytochemistry. RNA was extracted from the PlMEC samples and also from 3 term placenta and subjected to Affymetrix microarray analysis (U133Plus2 array chips). Data from the 3 term placentas and 3 preterm PlMEC arrays was used to generate an endothelial cell specific gene profile. This profile was used to identify the endothelial genes differentially regulated in all 6 IUGR cases. BTNL9 and NTRK2 transcripts were upregulated and SAA1, GNAS and SLAMF1 transcripts were downregulated as relative to the preterm controls. These changes were validated by Real time PCR in the PlMEC samples. This novel study is the first to identify endothelial candidate genes that may play a role in the villous hypoplasia of severe IUGR. This work advances our understanding of the molecular defects in placental microvascular endothelial cells in normal and pathologic pregnancies.
2012-04-01 | GSE25861 | GEO