Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Lipid metabolism genes in first trimester placenta

ABSTRACT: Placentas of obese women have low mitochondrial beta-oxidation of fatty acids (FA) and accumulate lipids in late pregnancy. This creates a lipotoxic environment, impairing placental efficiency. We assessed expression of key regulators of FA metabolism in first trimester placentas of lean and obese women. Expression of genes associated with FA oxidation (FAO; ACOX1, CPT2, AMPKα), FA uptake (LPL, LIPG, MFSD2A), FA synthesis (ACACA) and storage (PLIN2) were significantly reduced in placentas of obese compared to lean women. This effect was exacerbated in placentas of male fetuses. The PPARα pathway was enriched for placental genes impacted by obesity. These results demonstrate that obesity and hyperlipidemia impact placental FA metabolism as early as 7 weeks of pregnancy.

ORGANISM(S): Homo sapiens

PROVIDER: GSE206037 | GEO | 2022/10/12

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Investigation of placental gene expression in obese women exposed to Metformin during pregnancy

Project description:Maternal obesity in pregnancy is associated with increased birth-weight, obesity and premature mortality in adult offspring. The Effect of Metformin on Maternal and Fetal Outcomes in Pregnant Obese Women (EMPOWaR) trial was a randomised, double-blind, placebo-controlled trial carried out to determine whether exposure to Metformin would affect the offspring birth-weight centile. Obese women exposed to Metformin had increased insulin sensitivity at 36 weeks of pregnancy, but there were no differences in offspring birthweight. We obtained the placentas from these women to determine whether there were differences in expression of genes regulating fetal growth and metabolism. In a complementary study we investigated DNA methylation in the same samples.

2019-01-31 | E-MTAB-6418 | biostudies-arrayexpress

Maternal pre-pregnancy obesity is associated with altered placental transcriptome

Project description:Maternal obesity is becoming a major health consideration for successful pregnancy outcomes. There is growing proof that maternal obesity has a negative influence on placental development and function, thereby adversely influencing offspring programming and health outcomes. However, the molecular mechanisms underlying these processes are so far poorly understood. We set out to analyse term placenta whole transcriptome in obese (n=5) and normoweight women (n=5), using Affymetrix microarray platform compromising of 50,000 probe sets. Our analysis shows that the placental transcriptome differs between normoweight and obese women. Different processes and pathways among placenta from obese women were dysregulated, including inflammation and immune responses, lipid metabolism, cell death and survival and cancer pathways, vasculogenesis and angiogenesis, and glucocorticoid receptor signaling pathway. Together, this global gene expression profiling approach demonstrates and confirms that maternal obesity creates a unique in utero environment that impairs placental transcriptome.

2017-01-07 | E-MTAB-4541 | biostudies-arrayexpress

Investigation of placental DNA methylation in obese women exposed to Metformin during pregnancy

Project description:Maternal obesity in pregnancy is associated with increased birth-weight, obesity and premature mortality in adult offspring. The Effect of Metformin on Maternal and Fetal Outcomes in Pregnant Obese Women (EMPOWaR) trial was a randomised, double-blind, placebo-controlled trial carried out to determine whether exposure to Metformin would affect the offspring birth-weight centile. Obese women exposed to Metformin had increased insulin sensitivity at 36 weeks of pregnancy, but there were no differences in offspring birthweight. We obtained the placentas from these women to determine whether there were differences in DNA methylation of genes regulating fetal growth and metabolism. In a related study we investigated the gene expression in the same samples.

2018-11-01 | E-MTAB-6421 | biostudies-arrayexpress

Placental mRNA Expression data from pregnant smokers and non-smokers

Project description:We used microarrays to determine the transcriptional profiles of placental tissue obtained from women who smoked during pregnancy and from women who did not smoke during pregnancy. Fetal growth restriction is a frequent complication in mothers who smoke cigarettes during pregnancy. To evaluate novel pathways that regulate fetal growth affected by mothers who smoke, we isolated placental mRNA from smoking mothers with severe fetal growth restriction and compared them by microarray analysis to non-smoking mothers with appropriately grown fetuses. Bioinformatics analysis revealed distinct transcriptional patterns in the placentas of smoking mothers when compared to placentas from control non-smoking women. Analyses of the top upregulated and downregulated genes revealed several gene products such as secreted frizzled related protein 1 that was markedly upregulated in the placentas from women who smoked cigarettes during pregnancy. Total RNA was isolated from placental specimens obtained at time of delivery. RNA was hybridized to Affymetrix arrays, and analyzed.

2016-08-08 | E-GEOD-71931 | biostudies-arrayexpress

MeDIP and hMeDIP assays using human placentas of obese and lean (healthy weight) pregnancies

Project description:Maternal obesity has both a direct effect on the outcome of pregnancy but also programs the fetus for obesity and metabolic syndrome in later life. Due to its roles at the interface between mother and fetus, the placenta transduces and mediates the effects of the obese intrauterine environment on the fetus. Here we have generated genome-scale high-resolution maps of 5mC and 5hmC in human placentas of obese and healthy weight pregnancies. Widespread alterations to the placental epigenome identified across the genome in the setting of maternal adiposity are primarily characterized by increase in 5mC and reciprocal decrease in 5hmC. This is also evident at the two pregnancy-associated gene clusters on chromosomes 17 and 19. In addition, maternal adiposity is associated with downregulation of ten-eleven translocation (TET) and isocitrate dehydrogenase (IDH) family genes and is accompanied by decreased levels of Î±-ketoglutarate (Î±KG) in the placenta. Of note, Î±KG levels exhibit a close positive correlation with both ascorbate and aconitate levels and less substantial but significant association with global 5hmC levels and placenta-specific gene expression. These observations suggest a mechanistic linkage between obesogenic environment and conversion efficiency of 5mC to 5hmC and highlight the idea that TET-mediated active DNA demethylation pathway can sense and respond to metabolic derangements and plays a role in subsequent cellular adaptation. Collectively, this study demonstrates that altered DNA demethylation process is likely one of the mechanisms underlying metabolic modulation of the placental epigenome with maternal adiposity. Comparison of lean vs obese epigenomes in human pregnancies

2017-05-04 | E-GEOD-69769 | biostudies-arrayexpress

Placental mRNA Expression data from pregnant smokers and non-smokers

2016-08-08 | GSE71931 | GEO

Genome-wide analysis of uterine natural killer cell gene expression from lean and obese women in early pregnancy

Project description:Analysis of gene expression in uterine natural killer (NK) cells purified from either lean (control) or obese pregnanct women. The studys' aim is to identify differentially expressed genes and pathways in natural killer cells that are affected by maternal obesity. Results provide mechanitic insight into gene pathways altered in the condition of obeisty. Total RNA obtained from immuno-magnetic bead purified natural killer cells from uterine decidual mucosa from 7 to 10 week old pregnancies from 13 lean (BMI 20-24.9) and 11 obese (BMI >30) women. All women were between 19 and 35 years of age. In addition to BMI, blood serum CRP (hsCRP), a measure of inflammation, was measured via ELISA.

2016-06-15 | E-GEOD-75091 | biostudies-arrayexpress

AMPKα stimulates skeletal muscle fatty acid utilization during in vivo exercise in mice

Project description:Existing controversy regarding the importance of AMP-activated protein kinase (AMPK) in fatty acid (FA) oxidation in skeletal muscle with contraction/exercise may to some extent pertain to redundant AMPKα1 signaling. Using a mouse model lacking both AMPKα1 and -α2 in skeletal muscle specifically (mdKO) we hypothesized that FA utilization would be impaired in skeletal muscle. Calorimetric analysis showed a similar respiratory exchange ratio (RER) of AMPKα WT and mdKO mice when fed normal chow, a high fat diet or with prolonged fasting. Though, in vivo treadmill exercise at the same relative intensity induced a higher RER in mdKO mice compared to WT (WT=0.81; mdKO=0.87; p<0.01) indicating a decreased utilization of FA. Ex vivo incubation of soleus muscle revealed that basal and contraction-induced FA oxidation was impaired in mdKO mice, suggesting that the increased RER during in vivo running exercise originated from decreased skeletal muscle FA oxidation. A decreased muscle protein expression of CD36 and FABPpm (by 17-40%) together with abolishment of TBC1D1 Ser237 phosphorylation in mdKO mice, may result in lower FA transport capacity and FA transport protein translocation to sarcolemma, respectively. In summary this study shows that the catalytically active AMPKα subunits are required for normal stimulation of FA utilization during exercise and contractions.

2015-09-30 | GSE61904 | GEO

El-Bayoumy iTraq 8-plex Analysis of Human Female Plasma

Project description:This is a quantitative proteomic study of the plasma of obese versus lean post-menopausal women collected over a two-year time span, to establish whether Lovaza (a collection of omega-3 fatty acids) would alter protein biomarkers involved in lipogenesis, inflammation, immunity and carcinogenesis in Obese versus Lean women.

2019-07-23 | MSV000084125 | MassIVE

SARS-CoV-2 infection in pregnancy is associated with robust inflammatory response at the maternal-fetal interface

Project description:Pregnant women appear to be at increased risk for severe outcomes associated with COVID-19, but the pathophysiology underlying this increased morbidity and its potential impact on the developing fetus is not well understood. In this study of pregnant women with and without COVID-19, we assessed viral and immune dynamics at the placenta during maternal SARS-CoV-2 infection. Amongst uninfected women, ACE2 was detected by immunohistochemistry in syncytiotrophoblast cells of the normal placenta during early pregnancy but was rarely seen in healthy placentas at full term. Term placentas from women infected with SARS-CoV-2, however, displayed a significant increase in ACE2 levels. Using immortalized cell lines and primary isolated placental cells, we determined the vulnerability of various placental cell types to direct infection by SARS-CoV-2 in vitro. Yet, despite the susceptibility of placental cells to SARS-CoV-2 infection, viral RNA was detected in the placentas of only a subset (∼13%) of women in this cohort. Through single cell transcriptomic analyses, we found that the maternal-fetal interface of SARS-CoV-2-infected women exhibited markers associated with pregnancy complications, such as preeclampsia, and robust immune responses, including increased activation of placental NK and T cells and increased expression of interferon-related genes. Overall, this study suggests that SARS-CoV-2 is associated with immune activation at the maternal-fetal interface even in the absence of detectable local viral invasion. While this likely represents a protective mechanism shielding the placenta from infection, inflammatory changes in the placenta may also contribute to poor pregnancy outcomes and thus warrant further investigation.

2021-04-03 | GSE171381 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data