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Expression data of Myh6-MeCP2 transgenic mice

ABSTRACT: Hearts of Myh6-MeCP2 transgenic mice and wildtype littermates were rapidly dissected and flash frozen. We used Affymetrix microarrays to assess gene expression changes induced by overexpression of MeCP2 under the control of a cardiomycyte specific promoter. Hearts were dissected 2-3 weeks after birth from transgenic Myh6-MeCP2 mice and littermates to study gene expression alterations.

ORGANISM(S): Mus musculus

SUBMITTER: Ralf Gilsbach

PROVIDER: E-GEOD-52797 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Adrenergic Repression of the Epigenetic Reader MeCP2 Facilitates Cardiac Adaptation in Chronic Heart Failure.

Mayer Sandra C SC Gilsbach Ralf R Preissl Sebastian S Monroy Ordonez Elsa Beatriz EB Schnick Tilman T Beetz Nadine N Lother Achim A Rommel Carolin C Ihle Hannah H Bugger Heiko H Rühle Frank F Schrepper Andrea A Schwarzer Michael M Heilmann Claudia C Bönisch Ulrike U Gupta Shashi Kumar SK Wilpert Jochen J Kretz Oliver O von Elverfeldt Dominik D Orth Joachim J Aktories Klaus K Beyersdorf Friedhelm F Bode Christoph C Stiller Brigitte B Krüger Markus M Thum Thomas T Doenst Torsten T Stoll Monika M Hein Lutz L

Circulation research 20150720 7

<h4>Rationale</h4>In chronic heart failure, increased adrenergic activation contributes to structural remodeling and altered gene expression. Although adrenergic signaling alters histone modifications, it is unknown, whether it also affects other epigenetic processes, including DNA methylation and its recognition.<h4>Objective</h4>The aim of this study was to identify the mechanism of regulation of the methyl-CpG-binding protein 2 (MeCP2) and its functional significance during cardiac pressure o ...[more]

PMID: 26195221

Similar Datasets

Expression data of Myh6-MeCP2 transgenic mice

Project description:Hearts of Myh6-MeCP2 transgenic mice and wildtype littermates were rapidly dissected and flash frozen. We used Affymetrix microarrays to assess gene expression changes induced by overexpression of MeCP2 under the control of a cardiomycyte specific promoter.

2015-12-22 | GSE52797 | GEO

Differential gene expression in stellate sympathetic ganglia after cardiac pressure overload

Project description:Transcriptom analysis of stellate sympathetic ganglia after 8 weeks of cardiac pressure overload caused by transverse aortic constriction. Comparative transcriptome analysis was determined using the GeneChip Mouse Genome 430 2.0 Array (Affymetrix, Santa Clara, CA, USA). Six microarrays from stellate sympathetic ganglia of mice were performed 8 weeks after transverse aortic constriction or sham operation.

2010-02-25 | E-GEOD-18004 | biostudies-arrayexpress

Expression profile of COUP-TFII overexpressing hearts

Project description:Increased COUP-TFII levels are found in human dilated cardiomyopathy as well as in mouse models that develop cardiomyopathy. COUP-TFII overexpression in adult mouse hearts caused ventricular dilation and compromised cardiac functions. To gain insights on COUP-TFII’s effect in hearts, we identified the molecular profile of COUP-TFII overexpressing hearts through microarray analysis. The result may shred light on molecular mechanisms that mediate development of dilated cardiomyopathy. We utilized a previously established CAG-S-COUP-TFII allele and crossed it with the Myh6-MerCreMer (Myh6-MCM) line to overexpress COUP-TFII specifically in cardiomyocytes at two months of age by administration of tamoxifen. The experimental group has genotype of Myh6-MCM; CAG-S-COUP-TFII while the control group consists of Myh6-MCM mice (Figure 1C). Whole ventricles were harvested 16 days post induction for molecular profiling.

2015-07-24 | E-GEOD-63759 | biostudies-arrayexpress

Mus musculus

Project description:Expression data of Myh6-MeCP2 transgenic mice

| PRJNA230056 | ENA

E-GEOD-52797

Project description:Expression data of Myh6-MeCP2 transgenic mice

2016-04-07 | E-GEOD-52797 | ExpressionAtlas

Tumor Necrosis Factor Associated Factor 2 Mediates Cardiac Protection Through Non-canonical NF-κB Signaling

Project description:To elucidate the mechanisms responsible for cytoprotective effects of tumor necrosis factor receptor activated factor 2 (TRAF2) in the heart, we employed genetic gain and loss of function studies ex vivo and in vivo in mice with cardiac restricted overexpression of TRAF2 (Myh6-TRAF2LC). Crossing Myh6-TRAF2LC mice with mice lacking canonical signaling (Myh6-TRAF2LC/Myh6-IκBαΔN) abrogated the cytoprotective effects of TRAF2 ex vivo. In contrast, inhibiting the JAK/STAT pathway did not abrogate the cytoprotective effects of TRAF2. Transcriptional profiling of wild-type, Myh6-TRAF2LC, Myh6-TRAF2LC/Myh6-IκBαΔN hearts suggested that the non-canonical NF-κB signaling pathway was upregulated in the Myh6-TRAF2LC hearts. Western blotting and ELISA for the NF-κB family proteins p50, p65, p52 and RelB on nuclear and cytoplasmic extracts from naïve 12 week old wild-type, Myh6-TRAF2LC and Myh6-TRAF2LC/Myh6-IκBαΔN mouse hearts showed increased expression levels and increased DNA binding of p52 and RelB, which are NF-κB family members, whereas there was no increase in expression nor DNA binding of the p50 and p65 subunits. Crossing Myh6-TRAF2LCmice with RelB-/+mice (Myh6-TRAF2LC/RelB-/+) attenuated the cytoprotective effects of TRAF2 ex vivo and in vivo. Viewed together, these results suggest that cross-talk between the canonical and non-canonical NF-κB signaling pathways is required for mediating the cytoprotective effects of TRAF2.

2017-12-15 | GSE107668 | GEO

RNA-seq comparing the WT mouse hearts versus Dhx36 cKO hearts

Project description:This experiment aimed to investigate the transcriptional role of G4 resolvase Dhx36 in the adult mouse heart. We compared three pools of wild-type (WT) mouse hearts with three pools of Dhx36 conditional knockout (cKO) hearts. In the mutant mice, Dhx36 was conditionally deleted in cardiomyocytes using the Myh6-cre transgenic line. Each of the six pools was created using RNA extracted from 3-5 hearts from mice aged approximately 21 days. The cKO mice developed dilated cardiomyopathy and began experiencing sudden death at 40 days old, with no mutants surviving beyond 5 months.

2024-09-15 | E-MTAB-14440 | biostudies-arrayexpress

Cerebellar gene expression data from Mecp2-null and MECP2-transgenic mice

Project description:We compared gene expression changes in the cerebellum of mice lacking MeCP2 (Mecp2-null) and mice overexpressing MeCP2 (MECP2-transgenic). A group of postnatal neurodevelopmental disorders collectively referred to as MeCP2 disorders are caused by aberrations in the gene encoding methyl-CpG-binding protein 2 (MECP2). Loss of MeCP2 function causes Rett syndrome (RTT), whereas increased copy number of the gene causes MECP2 duplication or triplication syndromes. MeCP2 acts as a transcriptional repressor, however the gene expression changes observed in the hypothalamus of MeCP2 disorder mouse models suggest that MeCP2 can also upregulate gene expression. To determine if this dual role of MeCP2 extends beyond the hypothalamus, we studied gene expression patterns in the cerebellum of Mecp2-null and MECP2-Tg mice, modeling RTT and MECP2 duplication syndrome, respectively. We found that abnormal MeCP2 dosage causes alterations in the expression of hundreds of genes in the cerebellum. The majority of genes were upregulated in MECP2-Tg mice and downregulated in Mecp2-null mice, consistent with a role for MeCP2 as a modulator that can both increase and decrease gene expression. Interestingly, many of the genes altered in the cerebellum, particularly those increased by the presence of MeCP2 and decreased in its absence, were similarly altered in the hypothalamus. Keywords: Comparison of cerebellar gene expression data between Mecp2-null mice and Mecp2-transgenic mice Total cerebellar RNA samples were collected from Mecp2-null male mice (n=5), MECP2-transgenic male mice (n=5), and their wild type male littermates at 6 weeks of age (n=5 for each group).

2010-04-10 | E-GEOD-15574 | biostudies-arrayexpress

Hypothalamic gene expression data from Mecp2-null and MECP2-transgenic mice

Project description:We compared gene expression changes in the hypothalamus of mice lacking MeCP2 (Mecp2-null) and mice overexpressing MeCP2 (MECP2-transgenic). Mutations in the gene encoding the transcriptional repressor methyl-CpG binding protein 2 (MeCP2) cause the neurodevelopmental disorder Rett syndrome. Loss of function as well as increased dosage of MECP2 gene cause a host of neuropsychiatric disorders. To explore the molecular mechanism(s) underlying these disorders, we examined gene expression patterns in the hypothalamus of mice that either lack or overexpress MeCP2. In both models, MeCP2 dysfunction induced changes in the expression levels of thousands of genes, but surprisingly the majority of genes (~85%) appeared to be activated by MeCP2. We selected six genes and confirmed that MeCP2 binds to their promoters. Furthermore, we showed that MeCP2 associates with the transcriptional activator CREB1 at the promoter of an activated target but not a repressed target. These studies suggest that MeCP2 regulates the expression of a wide range of genes in the hypothalamus and that it can function as both an activator and repressor of transcription. Total hypothalamic RNA samples were collected from Mecp2-null male mice (n=4), MECP2-transgenic male mice (n=4), and their wild type male littermates at 6 weeks of age (n=4 for each group).

2008-05-30 | E-GEOD-11150 | biostudies-arrayexpress

Cell type specific expression data from Mecp2 null mice

Project description:Human methyl-CpG-binding protein 2 (MeCP2) disruption causes Rett syndrome, an autistic disease prevalent in females. Previous microarray expression profiling studies using tissue homogenate samples from mouse model of the Rett syndrome revealed only modest changes in expression caused by the loss of Mecp2, making it difficult to identify etiology of the Rett syndrome. Here, we carried out cell type specific genome wide expression profiling of Mecp2 null mice in three neuronal cell types. We found a hot spot of Mecp2 affected genes in chromosome 11B3 syntenic to human chromosome 17p13 which has known associations to mental retardation. We also found Mecp2 affected genes are almost non-overlapping between cell types. Cell-adhesion category of genes, however, are commonly overrepresented, suggesting a possible etiology of Rett syndrome Keywords: cell type comparison, disease state analysis, genetic modification Transgenic mice lines which label subpopulations of neurons (G42: fast spiking Parvarbumin positive interneurons, YFPH: layer 5 thick tufted pyramidal neurons, TH: tyrosine hydroxylase positive locus coeruleus neurons) were used to obtain cell type specific expression profiles on Affymetrix microarrays. Females which carry Mecp2 null alleles (and one of the fluorescent alleles) were crossed with males (which may or may not carry one of the fluorescent alleles depending on whether the female has one or not). Male offsprings at around age P40 which carry fluorescent allele and Mecp2 null allele were used for experiments. Littermate males which carry fluorescent allele but not Mecp2 null allele were used for controls. 3 or 4 biological replicates were done for each condition.

2011-11-01 | E-GEOD-8720 | biostudies-arrayexpress

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