Cardiac over-expression of Med13, non-cardiac tissue analysis
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE35903 | GEO | 2012/02/18
SECONDARY ACCESSION(S): PRJNA155689
REPOSITORIES: GEO
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Project description:Med13 cardiac over-expression regulates obesity. Liver, WAT and BAT from alphaMHC-Med13 TG mice was analyzed Liver, WAT and BAT from Med13 alphaMHC transgenic mice and wild type littermates
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Project description:Med13 cardiac over-expression regulates cardiac gene expression and metabolism Hearts from Med13 alphaMHC transgenic mice and wild type littermates
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Project description:Med13 cardiac over-expression regulates cardiac gene expression and metabolism
2012-02-18 | GSE35902 | GEO
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
2012-02-18 | E-GEOD-35904 | biostudies-arrayexpress
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
2019-05-15 | GSE124117 | GEO
Project description:Regulation of cardiac transcription by thyroid hormone and Med13
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Project description:Background: Brown and white adipose tissues (BAT and WAT) play critical roles in controlling energy homeostasis and in the development of obesity and diabetes. Fsp27 is expressed in both BAT and WAT and promotes lipid storage and the development of obesity and diabetes. In addition, Fsp27-deficient white adipocytes acquired certain BAT-like properties including reduced lipid droplet size and increased mitochondrial activity. Using microarray and semi-quantitative real-time PCR analyses, we systematically analyzed the gene expression profile in Fsp27-deficient WAT and BAT. Results: We observed that BAT-selective genes were significantly up-regulated, whereas WAT-selective genes were down-regulated in the WAT of Fsp27-/- mice. Expression levels of BAT-selective genes were also dramatically up-regulated in the WAT of leptin and Fsp27 double deficient mice. Furthermore, we observed that expression levels of genes in multiple metabolic pathways including oxidative phosphorylation, the TCA cycle and fatty acid synthesis and oxidation were increased in the Fsp27-/- WAT. In contrast, expression levels for extracellular matrix remodeling, the classic complement pathway and TGF-β signaling"were down-regulated in the WAT of Fsp27-/- mice. Most importantly, regulatory factors that determine BAT identity such as CEBPα/β, PRDM16 and major components in the cAMP pathway were markedly up-regulated in the WAT of Fsp27-/- mice. Interestingly, we observed distinct gene expression profiles in the BAT of Fsp27-/- mice. Conclusion: Our data suggest that Fsp27 acts at upstream to control gene expression of diverse pathways, in particular the expression of regulatory factors that determine the identity of BAT and WAT. Therefore, Fsp27 is an important molecular determinant for the identity of WAT, and loss of Fsp27 leads to the conversion of WAT to a BAT-like tissue. Total RNAs were extracted from individual gonadal WAT of five pairs of 3-month-old wild-type and Fsp27-null male mice. Equal amounts of RNA from five pairs of mice with each genotype were pooled to form RNA pools (total 45 μg). Duplicate experiments were carried out.
2010-07-07 | E-GEOD-22693 | biostudies-arrayexpress
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
Project description:Cardiac myocyte-specific ERalpha KO mice were generated to assess the role of ERα in the heart. Female ERαHKO mice displayed a modest cardiac phenotype, but unexpectedly, an the most striking obesity phenotype developed was obesity in female ERαHKO but not male ERαHKO mice. In female ERαHKO mice we identified cardiac dysfunction, mild glucose and insulin intolerance, and reduced ERα gene expression in skeletal muscle and white adipose tissue (WAT). RNA-seq analysis was conducted on the ventricles and WAT of male and female ERαHKO mice to further elucidate the transcriptomic alterations associated with the shift in metabolic profiles in the tissues of interest.
2023-01-24 | E-MTAB-12564 | biostudies-arrayexpress
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.
2020-12-29 | GSE147366 | GEO