Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The effect of sEV/miR-29a-3p on glucose metabolism in fetal rat liver

ABSTRACT: Obesity during pregnancy is linked to a high risk of offspring overweight, insulin resistance, type 2 diabetes, and cardiometabolic disease in later life. However, the underlying mechanisms by which maternal factors drive these long-lasting effects remain to be fully elucidated. In our study, we have demonstrated that in diet-induced-obesity (DIO) pregnant mice, maternal small extracellular vesicles (sEV) in circulating system have the ability to cross the placental barrier and reach the liver of fetal mice, exerting a sustained adverse impact on offspring insulin sensitivity. Further investigations have revealed that pathogenically increased miR-29a-3p in maternal sEV from DIO mice can be delivered into livers of fetal offspring. Elevated miR-29a-3p subsequently alter epigenetic state in fetal liver via targeting several key methyltransferases and demethylases, interrupting the DNA methylation landscape, including hypomethylation of PGC-1α. Such epigenetic remodeling abnormally promotes early hepatic gluconeogenesis at fetal stage that contribute to the adult metabolic disturbance in offspring. Taken together, our finding suggests that the transplacental delivery of maternal sEV could serve as a potential mechanism for prenatal programming of metabolic health in offspring.

ORGANISM(S): Mus musculus

PROVIDER: GSE295756 | GEO | 2026/07/31

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Diet-induced obesity affects miRNAs expression in fetal mouse liver

Project description:Obesity during pregnancy is linked to a high risk of offspring overweight, insulin resistance, type 2 diabetes, and cardiometabolic disease in later life. However, the underlying mechanisms by which maternal factors drive these long-lasting effects remain to be fully elucidated. In our study, we have demonstrated that in diet-induced-obesity (DIO) pregnant mice, maternal small extracellular vesicles (sEV) in circulating system have the ability to cross the placental barrier and reach the liver of fetal mice, exerting a sustained adverse impact on offspring insulin sensitivity. Further investigations have revealed that pathogenically increased miR-29a-3p in maternal sEV from DIO mice can be delivered into livers of fetal offspring. Elevated miR-29a-3p subsequently alter epigenetic state in fetal liver via targeting several key methyltransferases and demethylases, interrupting the DNA methylation landscape, including hypomethylation of PGC-1α. Such epigenetic remodeling abnormally promotes early hepatic gluconeogenesis at fetal stage that contribute to the adult metabolic disturbance in offspring. Taken together, our finding suggests that the transplacental delivery of maternal sEV could serve as a potential mechanism for prenatal programming of metabolic health in offspring.

2026-07-31 | GSE298821 | GEO

Diet-induced obesity affects miRNA expression in plasma extracellular vesicles of pregnant mice

2026-07-31 | GSE297729 | GEO

miR-29a-3p affects DNA methylation level in fetal mouse liver

2026-07-31 | GSE299405 | GEO

Diet-induced obesity affects miRNA expression in plasma extracellular vesicles of pregnant women

2026-07-31 | GSE295983 | GEO

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

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

Identification and Comparative Analyses of Myocardial miRNAs Involved in Fetal Response to Maternal Obesity

Project description:Maternal obesity programs the offspring to cardiovascular disease, insulin resistance, and obesity. We sequenced and profiled the cardiac miRNAs that were dysregulated in the hearts of baboon fetuses born to a high fat / high fructose diet fed mothers compared to a regular diet fed mothers. Fetal hearts were collected from baboon fetuses born to obese and lean mothers, total RNA was isolated, and fetal cardiac miRNA were sequenced and profiled

2013-02-01 | E-GEOD-43323 | biostudies-arrayexpress

Sexually Dimorphic Regulation of MiR-29a/c-3p in Human Endothelial Cells: Cell Functions and Transcriptome

Project description:Preeclampsia (PE) is a major cause of maternal and fetal morbidity and mortality during pregnancy. PE is characterized by widespread endothelial dysfunction in mothers and fetuses. To date, the etiology of PE remains elusive, but the dysregulation of microRNAs (miRNAs) in endothelial cells may contribute to the pathogenesis of PE. We have reported that PE downregulates expression of two miRNAs, miR-29a-3p and miR-29c-3p (miR-29a/c-3p) and knockdown of miR-29a/c-3p impairs functions of human umbilical vein endothelial cells (HUVECs). Herein, we tested the hypothesis that knockdown of miR-29a/c-3p sex-specifically impairs cellular responses to vascular endothelial growth factor-A (VEGFA) and fibroblast growth factor 2 (FGF2) accompanying with disrupted transcriptome in HUVECs. MiR-29a/c-3p were downregulated using miR-29c-3p inhibitors in HUVECs, followed by assessing chemotactic and proliferative responses to VEGFA and FGF2. RNA-seq analysis was conducted to profile transcriptomic changes. Compared with negative control, miR-29c-3p inhibitors suppressed over 90% of miR-29a/c-3p in HUVECs at 48 h. MiR-29c-3p inhibitors decreased VEGFA-stimulated chemotaxis by 25% in male, but not female HUVECs. MiR-29c-3p inhibitors did not alter FGF2-stimulated chemotaxis or VEGFA- and FGF2-stimulated proliferation in HUVECs. RNA-seq revealed that miR-29a/c-3p inhibitors differentially altered the transcriptome between female and male HUVECs. Functional enrichment analyses showed that miR-29a/c-3p-regulated genes were differently associated with hypertension, heart, angiogenesis, and immunology in female and male HUVECs. These data demonstrate that knockdown of miR-29a/c-3p differentially affects cellular responses to angiogenic factors in female and male HUVECs, in association with disrupted transcriptome. These miR-29a/c-3p-regulated genes might serve as sex-specific therapeutic targets for PE-associated vascular dysfunction.

2026-05-28 | GSE310550 | GEO

Microarray data from e4.5 mouse trophectoderm on high fat vs control diet

Project description:Maternal obesity can lead to altered outcomes for offspring, and it is believed that the placenta plays a role in this fetal programming. We sought to examine the effects on maternal diet-induced obesity on changes in gene expression at the earliest stages of placenta development using microarray

2017-08-04 | GSE102241 | GEO

Hofbauer cells and fetal brain microglia share transcriptional profiles and responses to maternal diet-induced obesity

Project description:Maternal immune activation is associated with adverse offspring neurodevelopmental outcomes, many mediated by in utero microglial programming. As microglia remain inaccessible throughout development, identification of noninvasive biomarkers reflecting fetal brain microglial programming could permit screening and intervention. We used lineage tracing to demonstrate the shared ontogeny between fetal brain macrophages (microglia) and fetal placental macrophages (Hofbauer cells) in a mouse model of maternal diet-induced obesity, and single-cell RNA-seq to demonstrate shared transcriptional programs. Comparison with human datasets demonstrated conservation of placental resident macrophage signatures between mice and humans. Single-cell RNA-seq identified common alterations in fetal microglial and Hofbauer cell gene expression induced by maternal obesity, as well as sex differences in these alterations. We propose that Hofbauer cells, which are easily accessible at birth, provide novel insights into fetal brain microglial programs, and may facilitate the early identification of offspring vulnerable to neurodevelopmental disorders in the setting of maternal exposures.

2024-06-05 | GSE252343 | 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