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Cardiac over-expression of Med13

ABSTRACT: Med13 cardiac over-expression regulates cardiac gene expression and metabolism

ORGANISM(S): Mus musculus

PROVIDER: GSE35902 | GEO | 2012/02/18

SECONDARY ACCESSION(S): PRJNA155687

REPOSITORIES: GEO

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Cardiac over-expression of Med13

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2012-02-18 | E-GEOD-35902 | biostudies-arrayexpress

Cardiac over-expression of Med13, non-cardiac tissue analysis

Project description:Med13 cardiac over-expression regulates obesity. Liver, WAT and BAT from alphaMHC-Med13 TG mice was analyzed

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Med13 overexpression

Project description:This SuperSeries is composed of the following subset Series: GSE35902: Cardiac over-expression of Med13 GSE35903: Cardiac over-expression of Med13, non-cardiac tissue analysis Med13 cardiac transgenic mice were back-crossed 4 or more generations to C57Bl6 mice. Refer to individual Series

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Regulation of cardiac transcription by thyroid hormone and Med13

Project description:Purpose: The objective of this study was to determine cardiac transcriptional pathways regulated in response to 1.) hypothyroidism and re-establishment of a euthyroid state and 2.) Med13-dependent cardiac transcriptional pathways regulated in response to hypothyroidism and re-establishment of a euthyroid state

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Regulation of cardiac transcription by thyroid hormone and Med13

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Mus musculus

Project description:Cardiac over-expression of Med13

| PRJNA155687 | ENA

Mus musculus

Project description:Cardiac over-expression of Med13, non-cardiac tissue analysis

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RNA sequencing of HAP1 WT and MED13 KO clones

Project description:Purpose: The aim of the experiment was to eludicate differentialy expressed genes (DEGs) upon treatment with alkylating agent MMS between WT and MED13 deficient HAP1 cells. Results: After bioinformatic processing, at ≥2-fold change and an FDR≤0.1, 446 DEGs were identified in MED13 KO cells when compared to WT. Upon the MMS treatment 394 DEGs were identified in MED13 KO cells, of which 229 were common with untreated MED13 KO cells. Conclusions: Common DEGs represented genes directly regulated by MED13.

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MED13cTg heart ventricles and epididymal fat

Project description:The heart requires a continuous supply of energy but has little capacity for energy storage and thus relies on exogenous metabolic sources. We previously showed that cardiac MED13 modulates systemic energy homeostasis in mice. Here we sought to define the extra-cardiac tissue(s) that respond to cardiac MED13 signaling. We show that cardiac over-expression of MED13 in transgenic (MED13cTg) mice confers a lean phenotype that is associated with increased lipid uptake, beta-oxidation and mitochondrial content in white adipose tissue (WAT) and liver. Cardiac expression of MED13 decreases metabolic gene expression and metabolite levels in heart and liver but enhances them in WAT. Although exhibiting increased energy expenditure in the fed state, MED13cTg mice metabolically adapt to fasting. Furthermore, MED13cTg hearts oxidize fuel that is readily available, rendering them more efficient in the fed state. Parabiosis experiments in which circulations of wild-type and MED13cTg mice are joined, reveal that circulating factor(s) in MED13cTg mice promote enhanced metabolism and leanness. These findings demonstrate that MED13 acts within the heart to promote systemic energy expenditure in extra-cardiac energy depots and point to an unexplored metabolic communication system between the heart and other tissues.

2014-12-01 | GSE62450 | GEO

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