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Cardiac energy dependence on glucose activates metabolic genes controlled by mTOR

ABSTRACT: Mice lacking the expression of Acsl1 in the heart (Acsl1H-/-) have impaired cardiac fatty acid oxidation and develop spontaneous cardiac hypertrophy due to increased mTOR activation. To explore how the loss of ACSL1 alters gene expression, we performed a global gene expression analysis on ventricular RNA isolated from Acsl1H-/- and Acsl1flox/flox mice ten weeks after tamoxifen treatment when ACSL1 protein is completely lost and the specific activity of ACSL1 in Acsl1H-/- hearts is reduced 90%

ORGANISM(S): Mus musculus

PROVIDER: GSE51913 | GEO | 2014/09/29

SECONDARY ACCESSION(S): PRJNA225803

REPOSITORIES: GEO

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Cardiac energy dependence on glucose activates metabolic genes controlled by mTOR

Project description:Mice lacking the expression of Acsl1 in the heart (Acsl1H-/-) have impaired cardiac fatty acid oxidation and develop spontaneous cardiac hypertrophy due to increased mTOR activation. To explore how the loss of ACSL1 alters gene expression, we performed a global gene expression analysis on ventricular RNA isolated from Acsl1H-/- and Acsl1flox/flox mice ten weeks after tamoxifen treatment when ACSL1 protein is completely lost and the specific activity of ACSL1 in Acsl1H-/- hearts is reduced 90% Two-condition experiment, cadiac gene expression of Acsl1H-/- vs Acsl1flox/flox mice 10 weeks after tamoxifen treatment. Biological replicates: 3-4 per condition.

2014-09-29 | E-GEOD-51913 | biostudies-arrayexpress

Metabolic and Transcriptional Alterations in the Early Stages of Cardiac Fuel Switch Hint at Novel mTOR-mediated Regulation of Hypertrophy [RNA-seq]

Project description:1. Background- Long-chain acyl-CoA synthetases (ACSL) catalyze the conversion of long-chain fatty acids (FA) to fatty acyl-CoAs. Cardiac-specific ACSL1 knockout results in a shift towards glycolysis that promotes mTORC1-mediated ventricular hypertrophy. We used unbiased metabolomics and gene expression analyses to examine the early effects of genetic inactivation of FA oxidation on cardiac metabolism and function. 2. Methods and Results- Compared to WT hearts, global cardiac transcriptional analysis revealed differential expression of 245 genes in Acsl1H-/- hearts 2 weeks after Acsl1 ablation. Comparison of the 2- and 10-week transcriptional responses uncovered 139 genes whose expression was uniquely changed upon short-term cardiac inactivation of ACSL1. In particular, partial ACSL1 ablation led to the distinct upregulation of fibrosis genes, a phenomenon not observed after complete ACSL1 knockout. Metabolomic analysis identified 65 metabolites altered in hearts displaying partially reduced ACSL activity, whereas rapamycin treatment normalized the cardiac metabolomic fingerprint. Chronic mTOR inhibition via rapamycin treatment revealed novel mTORC1 targets involved in fibrosis, amino acid catabolism, and mitochondrial transport and metabolism. 3. Conclusions- Short-term cardiac-specific ACSL1 inactivation (Acsl1H-/-) resulted in metabolic and transcriptional derangements distinct from those observed upon complete ACSL1 knockout, leading to the identification of novel mTORC1 targets that regulate cardiac hypertrophy development, and suggesting heart-specific mTOR signaling that occurs during the early stages of substrate switching. Moreover, the rate of increased glucose use correlated negatively with hypertrophy development, strongly suggesting that hearts do not become hypertrophied if they can compensate or switch faster from FA to glucose use.

2018-04-27 | GSE103863 | GEO

Metabolic and Transcriptional Alterations in the Early Stages of Cardiac Fuel Switch Hint at Novel mTOR-mediated Regulation of Hypertrophy [Agilent Expression]

2018-04-27 | GSE103376 | GEO

Impact of IRP deficiency on the proteome of Ly6G+ cells from the bone marrow in mice

Project description:The overall objective of the project is to evaluate the effects of loss of function of iron regulatory proteins (IRP1, encoded by Aco1)-1 and -2 (IRP2, encoded by Ireb2) during adult life. Mice carrying floxed Aco1 and Ireb2 alleles were crossed to a knockin strain expressing a tamoxifen-inducible CRE recombinase under the control of the Rosa26 promoter. The resulting Aco1flox/flox,Ireb2flox/flox,Rosa26+/CreERT2 mice are designated P1/2-KO; littermates lacking the CreER sequence (Aco1flox/flox,Ireb2flox/flox,Rosa26+/+) serve as reference and are designated P1/2-CTR. Adult mice were injected (i.p.) with tamoxifen on day 1 and day 3 to ablate the IRPs in the whole body, and were sacrificed on day 10 for analysis. Bone marrow cells were collected and LY6G+ cells were magnetically sorted for proteome analysis by LC-MS/MS using an Ultimate 3000 UPLC system connected to an Orbitrap Exploris 480 mass spectrometer.

2023-03-11 | PXD032077 | Pride

Brown Adipose YY1 Deficiency Activates Expression of Secreted Proteins Linked to Energy Expenditure and Prevents Diet-Induced Obesity [IWAT]

Project description:Analysis of subcutaneous adipose tissue (IWAT) from Yin Yang 1 brown fat specific knockout mice fed a high fat diet for 2 weeks. The goal was to identify a gene signature of IWAT browning in YY1 mutant mice. Control mice YY1flox/flox versus YY1flox/flox; Ucp1Cre were fed a high fat diet for 2 weeks

2015-11-10 | E-GEOD-68382 | biostudies-arrayexpress

Targeting Cytoplasmic SAM by Expressing Slc25a26 Inhibits Protein Synthesis in Cardiac Hypertrophy via SAMTOR/mTOR signaling

Project description:Excess protein synthesis is the major pathological manifestation of cardiac hypertrophy; however, the underlying mechanism remains elusive. Here we found that a SAM transporter Slc25a26 translocated to mitochondria during cardiac hypertrophy. Silencing Slc25a26 aggravated phenylephrine-induced cardiomyocyte hypertrophy in neonatal rat ventricular myocytes. Transcriptome analysis revealed a specific regulation of ribosome genes by Slc25a26. Puromycin incorporation assay showed a negative regulation of protein synthesis rate by Slc25a26. The translational regulation was independent of ribosome assembly, but abolished by mTOR inhibitor rapamycin. Administration of SAM, or silencing Samtor, reversed the inhibitory impact of Slc25a26 on protein synthesis. AAV9-mediated Slc25a26 overexpression in mouse heart increased the SAM level in mitochondria, but reduced that in nucleus and cytoplasm. Transaortic-constriction-induced hypertrophic pathologies, including pathological gene induction, cardiomyocyte enlargement, myocardial remodeling and heart dysfunction were significantly alleviated by Slc25a26 overexpression. Our data demonstrate a crucial role of subcellular SAM homeostasis in translational control during cardiac hypertrophy.

2022-01-05 | GSE173737 | GEO

Brown Adipose YY1 Deficiency Activates Expression of Secreted Proteins Linked to Energy Expenditure and Prevents Diet-Induced Obesity [BAT]

Project description:Analysis of brown adipose tissue from Yin Yang 1 (YY1) brown fat specific knockout mice fed a high fat diet for 3 months. YY1 deficiency in brown adipose tissue leads to strong thermogenic deficiency. The goal was to identify the genes controlled by YY1 responsible of brown fat defective function. Control mice YY1flox/flox versus YY1flox/flox; Ucp1Cre were fed a high fat diet for 3 months

2015-11-10 | E-GEOD-68429 | biostudies-arrayexpress

RNA-seq of mouse glioma tumors with or without ASCL1

Project description:Tamoxifen was administered to Glast-CreER;Nf1-flox/flox;Tp53-flox/flox or Glast-CreER;Ascl1-flox/flox;Nf1-flox/flox;Tp53-flox/flox at E14.5 to induce tumors in the brain

2020-11-05 | GSE152400 | GEO

Gene profiling of Hand2 target genes and transcriptional regulation of Hand2 expression in the postnatal myocardium

Project description:In humans, cardiac hypertrophy is the principal risk factor for the development of overt heart failure and sudden cardiac death from lethal arrhythmias. Although aberrant reactivation of fetal² gene programs is intricately linked to maladaptive hypertrophy of postnatal cardiomyocytes, loss of cardiac function and heart failure, the transcription factors driving these gene programs remain ill defined. We report that the basic helix-loop-helix (bHLH) transcription factor dHAND/Hand2 is re-expressed in the mammalian postnatal myocardium in response to stress signaling. Interestingly, mutant mice overexpressing Hand2 in otherwise healthy ventricular myocytes developed a phenotype of pathological hypertrophy. In contrast, conditional gene-targeted Hand2 mice demonstrated a marked resistance to pressure overload-induced hypertrophy, fibrosis, ventricular dysfunction and induction of a fetal gene program. These data suggest a critical role for the Hand2 transcription factor during hypertrophic remodeling and heart failure. To gain more mechanistically insight in the processes underlying heart failure, we here identified Hand2 target genes by microarray gene expression profiling. RNA samples were collected 4 weeks after sham or TAC surgery (to induce pressure overload) of both tamoxifen-treated Hand2f/f (WT) and MCM-Hand2f/f (KO) mice.

2013-11-15 | E-MTAB-1821 | biostudies-arrayexpress

Gene expression changes in Apc-mutant mouse intestinal organoids with and without deleting the Prox1 transcription factor

Project description:We isolated and selected intestinal adenoma organoids from villin-CreER; Apcflox/flox and villin-CreER; Apcflox/flox; Prox1flox/flox mice and added tamoxifen to induce the deletion of the Apc and Prox1 genes in the intestinal epitheliul ex vivo. Microarray experiments were carried out 7 days after the addition of tamoxifen. Total RNA obtained from villin-CreER; Apcflox/flox and villin-CreER; Apcflox/flox; Prox1flox/flox organoids were compared 7 days after the addition of tamoxifen and 5 days after the selection for Apc-mutant organoids in the absence of the Wnt-agonist R-Spondin1.

2014-08-15 | E-GEOD-47568 | biostudies-arrayexpress

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