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γ-Linolenic acid in maternal milk drives cardiac metabolic maturation

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE188991 | GEO | 2023/02/15

REPOSITORIES: GEO

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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

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

Parkin-mediated mitophagy evokes perinatal cardiac mitochondria maturation

2015-12-04 | GSE68921 | GEO

Perinatal cardiomyocyte maturation reference isolated by large-particle fluorescence activated cell sorting

Project description:To date, there have been limited high quality libraries of cardiomyocyte maturation during the perinatal period, in part owing to the difficulty of isolating large perinatal cardiomyocytes. We previously developed a method utilizing large-particle fluorescent activated cell sorting (LP-FACS) to isolate adult cardiomyocytes for single cell RNA-seq (Kannan et al., Circ Res, 2019). We utilize this method to generate a reference of perinatal cardiomyocyte maturation.

2020-04-01 | GSE147807 | GEO

Parkin-mediated mitophagy evokes perinatal cardiac mitochondria maturation

Project description:Exclusion of Parkin from mitochondria of perinatal cardiomyocytes interrupts structural and molecular transformations essential to normal perinatal-adult mitochondrial replacement. mRNA-sequencing from cardiac total RNA was performed at P1, P21 and 5-week stages of nontransgenic (ntg) and human-Mfn2-overexpressing (Mfn2wt) hearts, and also of tet-off control (tetoff) and human-Mfn2 T111A/S442A-overexpressing (Mfn2AA) hearts. Libraries from all P1 samples were prepared and analyzed together, and similarly all P21 libraries, and all 5-week libraries together. To facilitate comparison across time points by accounting for batch effect, new libraries were prepared starting from total RNA from selected P21 ntg and 5-week ntg hearts subjected to prior analysis, during the same batch preparation as all P1 samples, and analyzed together. Correction for differences observed between libraries prepared from the same total RNA, but at different times, allows comparison across timepoints.

2015-12-04 | E-GEOD-68921 | biostudies-arrayexpress

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

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