Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Metabolic maturation of neonatal hearts driven by γ-linolenic acid in maternal milk [ATAC-seq]

ABSTRACT: The goal of this study was to compare the epigenetic landscape of perinatal hearts of cardiomyocyte-specific RXRab-deficient (edKO) and WT mice, to identify differential chromatin dynamics that are controlled by TF RXRa and RXRb.

ORGANISM(S): Mus musculus

PROVIDER: GSE188997 | GEO | 2023/02/15

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Metabolic maturation of neonatal hearts driven by γ-linolenic acid in maternal milk [H3K27ac ChIP-seq]

Project description:The goal of this study was to compare the cistrome profile of H3K27ac (ChIP-seq) of perinatal hearts of cardiomyocyte-specific RXRab-deficient and WT mice, in order to identify genomic regions that are differentially activated by TF RXRa and RXRb.

2023-02-15 | GSE188996 | GEO

Metabolic maturation of neonatal hearts driven by γ-linolenic acid in maternal milk [RXR ChIP-seq]

Project description:The goal of this study was to compare the cistrome profile of RXR (ChIP-seq) of perinatal hearts of cardiomyocyte-specific RXRab-deficient and WT mice, in order to identify genomic regions which are directly controlled by TF RXRa and RXRb.

2023-02-15 | GSE188994 | GEO

γ-Linolenic acid in maternal milk drives cardiac metabolic maturation

Project description:The goal of this study was to compare the transcriptome profile (RNA-seq) of perinatal hearts of cardiomyocyte-specific RXRab-deficient (edKO) and WT mice, to identify genes that are controlled by the expression of the TF RXRa and RXRb.

2023-02-15 | GSE188991 | GEO

Metabolic maturation of neonatal hearts driven by γ-linolenic acid in maternal milk

Project description:Birth is the first metabolic challenge that cardiomyocytes need to overcome as they reshape their fuel preference from glucose to fatty acids (FA) to optimize energy production in postnatal life. This adaptation is partly triggered by drastic post-partum environmental changes, yet the molecular players responsible for orchestrating cardiomyocyte maturation remain unknown. Here, we discover that maternal metabolite γ-linolenic acid (GLA) support this transition. Specifically, colostrum GLA acts as an agonist for Retinoid X Receptors (RXR), a family of ligand-activated transcription factors expressed from embryonic life in cardiomyocytes. Mice lacking RXR in embryonic cardiomyocytes showed an aberrant chromatin landscape that prevented the induction of RXR-dependent FA metabolism genes (mtFAH signature). This results in a defective metabolic transition with blunted mitochondrial lipid-derived energy production and enhanced glucose consumption, which ultimately leads to perinatal lethal cardiac dysfunction. In vitro GLA supplementation in cardiomyocytes induced the expression of mtFAH signature in a RXR-dependent manner. Altogether, our study uncovers GLA/RXR axis as the fundamental mechanism by which maternal physiology commands metabolic functioning in perinatal hearts. This SuperSeries is composed of the SubSeries listed below.

2023-02-15 | GSE188998 | GEO

Retinoid X receptor promotes hematopoietic stem cell fitness and quiescence and preserves hematopoietic homesotasis [Single Cells]

Project description:Hematopoietic stem cells (HSCs) balance self-renewal and differentiation to maintain hematopoietic fitness throughout life. In steady-state conditions, HSC exhaustion is prevented by the maintenance of most HSCs in a quiescent state, with cells entering the cell cycle only occasionally. HSC quiescence is regulated by retinoid and fatty-acid ligands of transcriptional factors of the nuclear retinoid X receptor (RXR) family. Here, we show that dual deficiency for hematopoietic RXRa and RXRb induces HSC exhaustion, myeloid cell/megakaryocyte differentiation, and myeloproliferative-like disease. RXRa and RXRb maintain HSC quiescence, survival, and chromatin compaction; moreover, transcriptome changes in RXRa;RXRb-deficient HSCs include premature acquisition of an aging-like HSC signature, MYC pathway upregulation, and RNA intron retention. Fitness loss and associated RNA transcriptome and splicing alterations in RXRa;RXRb-deficient HSCs are prevented by Myc haploinsufficiency. Our study reveals the critical importance of RXRs for the maintenance of HSC fitness and their protection from premature aging.

2022-11-11 | GSE191162 | GEO

Retinoid X receptor promotes hematopoietic stem cell fitness and quiescence and preserves hematopoietic homesotasis [Bulk]

2022-11-11 | GSE191161 | GEO

RXRs are required for neonatal expansion of the serosal macrophage pool and contribute to ovarian cancer progression

Project description:Distinct macrophage populations throughout the body display highly heterogeneous transcriptional and epigenetic programs. However, the regulation of chromatin accessibility of tissue-resident macrophages is poorly understood. In this study, we generated a data set for genome-wide transposase-accessible chromatin analysis (ATAC-seq) of large peritoneal macrophages in animals with myeloid-specific double deletion of the nuclear receptors RXRa and RXRb.

2020-03-02 | GSE129414 | GEO

Gamma-linolenic acid, Dihommo-gamma linolenic, Eicosanoids and Inflammatory Processes.

Project description:Gamma-linolenic acid (GLA, 18:3n-6) is an omega-6 (n-6), 18 carbon (18C-) polyunsaturated fatty acid (PUFA) found in human milk and several botanical seed oils and is typically consumed as part of a dietary supplement. While there have been numerous in vitro and in vivo animal models which illustrate that GLA-supplemented diets attenuate inflammatory responses, clinical studies utilizing GLA or GLA in combination with omega-3 (n-3) PUFAs have been much less conclusive. A central premise of this review is that there are critical metabolic and genetic factors that affect the conversion of GLA to dihommo-gamma linolenic acid (DGLA, 20:3n-6) and arachidonic acid (AA, 20:4n-6), which consequently affects the balance of DGLA- and AA- derived metabolites. As a result, these factors impact the clinical effectiveness of GLA or GLA/(n-3) PUFA supplementations in treating inflammatory conditions. Specifically, these factors include: 1) the capacity for different human cells and tissues to convert GLA to DGLA and AA and to metabolize DGLA and AA to bioactive metabolites; 2) the opposing effects of DGLA and AA metabolites on inflammatory processes and diseases; and 3) the impact of genetic variations within the fatty acid desaturase (FADS) gene cluster, in particular, on AA/DGLA ratios and bioactive metabolites. We postulate that these factors influence the heterogeneity of results observed in GLA supplement-based clinical trials and suggest that "one-size fits all" approaches utilizing PUFA-based supplements may no longer be appropriate for the prevention and treatment of complex human diseases.

| S-EPMC4975646 | biostudies-literature

Gene expression changes in beta-blocker treated neonatal hearts

Project description:The regeneration potential of the mammalian heart is limited. We found that treatment of beta-blocker robustly enhanced cardiomyocyte proliferation and promoted cardiac regeneration post myocardial infarction. To investigate the gene expression changes, we performed RNA-seq using the hearts treated with beta-blocker for 7 days.

2022-08-30 | GSE186099 | GEO

Single cell ATAC-seq of cardiomyocytes from neonatal mouse hearts after injury

Project description:The adult mammalian heart is incapable of regeneration following injury. In contrast, the neonatal mouse heart has a transient ability to regenerate, however the molecular mechanism that mediates this regenerative response is not fully understood. Here, by single-nucleus RNA sequencing we map the transcriptome landscape of cardiomyocytes in neonatal mouse hearts at healthy, regenerative, and remodeling conditions. We show that an immature cardiomyocyte population enters cell-cycle in response to injury. Absence of this cardiomyocyte population overtime is associated with the loss of the ability of the heart to regenerate. We show a defined injury response in these cardiomyocytes, including activation of transcription factors NFYa and NFE2L1, which play proliferative and protective roles, respectively. We further show that overexpression of these two factors in vivo promotes heart regeneration. Thus, these findings refined our understanding of cellular basis of neonatal heart regeneration and reveal dynamic transcriptome landscape of cardiomyocytes in response to injury.

2020-03-18 | GSE142365 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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