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γ-Linolenic acid in maternal milk drives cardiac metabolic maturation

ABSTRACT: γ-Linolenic acid in maternal milk drives cardiac metabolic maturation

PROVIDER: PRJNA780956 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16960908.fastq.gz	Fastqsanger.gz
	SRR16960909.fastq.gz	Fastqsanger.gz
	SRR16960910.fastq.gz	Fastqsanger.gz
	SRR16960911.fastq.gz	Fastqsanger.gz
	SRR16960912.fastq.gz	Fastqsanger.gz

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

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

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

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

| PRJNA780976 | ENA

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

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

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

| PRJNA780975 | ENA

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

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

| PRJNA780967 | ENA

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 [ATAC-seq]

Project description: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.

2023-02-15 | GSE188997 | GEO

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

Maternal hematopoietic TNF, via milk chemokines, programs hippocampal development and memory

Project description:TNF is a proinflammatory cytokine with established roles in host defense and immune system organogenesis. Here we report a novel physiological function of TNF that extends its effect beyond the host into the developing offspring. A partial/complete maternal TNF-deficit, specifically in hematopoietic cells, resulted in reduced milk levels of chemokines IP-10, MCP-1/-3/-5, and MIP-1β, which in turn, augmented offspring postnatal hippocampal proliferation, leading to improved adult spatial memory. These effects were reproduced by the postpartum administration of a clinically used anti-TNF agent. Chemokines, fed to suckling pups of TNF-deficient mothers, restored both postnatal proliferation and adult spatial memory to normal levels. This work identifies a TNF-dependent “lactrocrine” pathway that programs offspring hippocampal development and memory. The level of ambient TNF is known to be downregulated by physical activity/exercise and adaptive stress; thus, we propose that the maternal TNF-milk chemokine pathway evolved to promote offspring adaptation to post-weaning environmental challenges/competition. Examined transcriptomes of TNF wild type offspring of TNF wild type or heterozygouse mothers

2013-12-01 | E-GEOD-52069 | biostudies-arrayexpress

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