Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

ACSS2 mediates an epigenetic pathway to regulate maternal Beta-cell adaptation and progression of gestational diabetes

ABSTRACT: ACSS2 mediates an epigenetic pathway to regulate maternal Beta-cell adaptation and progression of gestational diabetes

PROVIDER: PRJNA1009847 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

ACSS2 mediates an epigenetic pathway to regulate maternal Beta-cell adaptation and progression of gestational diabetes (scRNA-Seq)

Project description:Maternal pancreatic Beta-cell state is adapted to accommodate gestation metabolism. Defects in this process may cause gestational diabetes mellitus (GDM), with risk factors including a high-calorie diet during pregnancy. However, the regulatory mechanism of maternal Beta-cell adaptation is largely unknown. Using single-cell transcriptome combining genetic analyses, we discovered a precise process of Beta-cell adaptation in mice which is associated with progression of metabolic stress-related Beta-cell dysfunction, increased acetyl-CoA biosynthesis, and gene element-specific histone acetylation. STAT3 recruits p300 to promote histone acetylation levels of pregnancy-associated genes, and Acetyl-CoA Synthetase 2 (ACSS2) enhances this process. High-fat feeding causes hyperacetylation of chromatin that is specifically opened during pregnancy, which results in overexpression of genes that impair Beta-cell functions and, consequently, hyperglycemia. However, these impairments can be rescued by Beta-cell-specific deletion of Acss2. Therefore, our study reveals a precise adaptation process in Beta-cells at the single-cell level during pregnancy and a specific epigenetic pathway that regulates this process. We also explain the epigenetic regulatory mechanism by which a high-fat diet can lead to GDM and identify ACSS2 as a potential molecular target for controlling the progression of GDM.

2025-01-26 | GSE241770 | GEO

ACSS2 mediates an epigenetic pathway to regulate maternal β-cell adaptation and progression of gestational diabetes (ATAC-ChIP and ChIP-Seq)

Project description:Maternal pancreatic β-cell state is adapted to accommodate gestation metabolism. Defects in this process may cause gestational diabetes mellitus (GDM), with risk factors including a high-calorie diet during pregnancy. However, the regulatory mechanism of maternal β-cell adaptation is largely unknown. Using single-cell transcriptome combining genetic analyses, we discovered a precise process of β-cell adaptation in mice which is associated with progression of metabolic stress-related β-cell dysfunction, increased acetyl-CoA biosynthesis, and gene element-specific histone acetylation. STAT3 recruits p300 to promote histone acetylation levels of pregnancy-associated genes, and Acetyl-CoA Synthetase 2 (ACSS2) enhances this process. High-fat feeding causes hyperacetylation of chromatin that is specifically opened during pregnancy, which results in overexpression of genes that impair β-cell functions and, consequently, hyperglycemia. However, these impairments can be rescued by β-cell-specific deletion of Acss2. Therefore, our study reveals a precise adaptation process in β-cells at the single-cell level during pregnancy and a specific epigenetic pathway that regulates this process. We also explain the epigenetic regulatory mechanism by which a high-fat diet can lead to GDM and identify ACSS2 as a potential molecular target for controlling the progression of GDM.

2025-01-26 | GSE241773 | GEO

ACSS2 mediates an epigenetic pathway to regulate maternal Beta-cell adaptation and progression of gestational diabetes (scRNA-Seq)

Project description:ACSS2 mediates an epigenetic pathway to regulate maternal Beta-cell adaptation and progression of gestational diabetes (scRNA-Seq)

| PRJNA1009841 | ENA

ACSS2 mediates an epigenetic pathway to regulate maternal β-cell adaptation and progression of gestational diabetes (ATAC-ChIP and ChIP-Seq)

Project description:ACSS2 mediates an epigenetic pathway to regulate maternal β-cell adaptation and progression of gestational diabetes (ATAC-ChIP and ChIP-Seq)

| PRJNA1009853 | ENA

ACSS2 mediates an epigenetic pathway to regulate maternal Beta-cell adaptation and progression of gestational diabetes

Project description:This SuperSeries is composed of the SubSeries listed below.

2025-01-26 | GSE241776 | GEO

Gestational diabetes and human amniocytes

Project description:Gestational diabetes and human amniocytes

| PRJNA632929 | ENA

Gestational diabetes and human amniocytes

Project description:Context: Context: Gestational diabetes (GDM) has profound effects on the intrauterine metabolic milieu and is linked to obesity and diabetes in offspring, but the mechanisms driving these effects remain largely unknown. Alterations gene expression in amniocytes exposed to GDM in utero may identify potential mechanisms leading to metabolic dysfunction later in life. Objective: Objective: To profile changes in the transcriptome in human amniocytes exposed to GDM Methods: A nested case-control study was performed in second trimeseter amniocytes matched for offspring sex, maternal race/ethnicity, maternal age, gestational age at amniocentesis, gestational age at birth and gestational diabetes status. Sex-specific RNA-sequencing was completed and gene expression changes were identified. Results: Expression of interferon-stimulated genes was increased in GDM amniocytes accounting for 6 of the top 10 altered genes (q<0.05). Enriched biological pathways in GDM anmiocytes included pathways involving inflammation, the interferon response, fatty liver disease, monogenic diabetes and atherosclerosis. Conclusion: In a unique repository of human amniocytes exposed to GDM in utero, trancriptome analysis identified enrichment of inflammation and interferon-related pathways.

2020-05-15 | GSE150621 | GEO

DNA methylation and gestational diabetes mellitus

Project description:DNA methylation and gestational diabetes mellitus

| PRJEB66494 | ENA

METTL3 mediates m6A modification of hsa_circ_0072380 to regulate the progression of gestational diabetes mellitus

Project description:METTL3 mediates m6A modification of hsa_circ_0072380 to regulate the progression of gestational diabetes mellitus

| PRJNA1053777 | ENA

RNAseq between gestational diabetes mellitus and healthy control groups

Project description:tsRNA profiles of gestational diabetes mellitus and healthy control groups were generated by deep sequencing using Illumina NextSeq 500.

2024-05-12 | GSE267259 | 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