Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

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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Publications

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

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Project description: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 MeCP2 dosage causes MECP2 duplication or triplication syndromes. MeCP2 acts as a transcriptional repressor, however, the gene expression changes observed in the hypothalamus and cerebellum of MeCP2 disorder mouse models suggest that MeCP2 can also upregulate gene expression. In this study, we compared gene expression changes in the amygdalae of mice lacking MeCP2 (Mecp2-null) and mice overexpressing MeCP2 (MECP2-TG). We chose the amygdala because it is a neuroanatomical region implicated in the control of anxiety and social behavior, two prominent phenotypes in MECP2-TG mice, and hypothesized that transcriptional profiling of this particular brain region may reveal expression changes relevant to heightened anxiety-like behavior and abnormal social behavior. A total of 1,060 genes were altered in opposite directions in both MeCP2 mouse models compared with wild-type littermates, with ~60% up-regulated and ~40% down-regulated. Interestingly, we found a significant enrichment of anxiety- and/or social behavior-related genes among the differentially expressed genes. To determine whether these genes contribute to the anxiety and social behavior phenotypes in MECP2-TG mice, we performed genetic and pharmacologic studies and found that a reduction in Crh suppresses anxiety-like behavior, and a reduction in Oprm1 improves social approach behavior. These studies suggest that MeCP2 impacts molecular pathways involved in anxiety and social behavior, and provide insight into potential therapies for MeCP2 disorders. This study is published in Nature Genetics http://dx.doi.org/10.1038/ng.1066. Total amygdala RNA samples were collected from Mecp2-null male mice (n=4), MECP2-transgenic male mice (n=5), and their wild type male littermates at 6 weeks of age (n=4, n=5 for each group respectively).

Dataset Information

Expression data of Myh6-MeCP2 transgenic mice

Publications

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

Similar Datasets

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