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Expression data from mouse heart with and without GATA4 S105A mutation; with and without adrenergic stress

ABSTRACT: Serine 105 phosphorylation of GATA4 is necessary for stress-induced cardiac hypertrophy in vivo. We used microarrays to detail global gene expression program alterations that arise in response to the ablation of the Gata4 S105 phosphorylation site in basal and adrenergic-stressed heart ventricles. Wildtype and genetically engineered mice were subjected to control or pseudoephedrine treatment and heart ventricle RNAs were extracted and hybridized on Affymetrix microarrays. Comparisons consisted of identifying treatment- and genotype-affected gene expression patterns.

ORGANISM(S): Mus musculus

SUBMITTER: Bruce Aronow

PROVIDER: E-GEOD-30314 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Expression data from mouse heart with and without GATA4 S105A mutation; with and without adrenergic stress

Project description:Serine 105 phosphorylation of GATA4 is necessary for stress-induced cardiac hypertrophy in vivo. We used microarrays to detail global gene expression program alterations that arise in response to the ablation of the Gata4 S105 phosphorylation site in basal and adrenergic-stressed heart ventricles.

2011-06-30 | GSE30314 | GEO

Parsing the roles of transcription factors Gata4 and Gata6 in adult cardiac hypertrophic responses

Project description:Cardiac hypertrophy is regulated by the zinc finger-containing DNA binding factors Gata4 and Gata6, both of which are required to mount a productive growth response of the adult heart. To determine if Gata4 and Gata6 are redundant or have non-overlapping roles, we performed cardiomyocyte-specific conditional gene deletions for Gata4 and Gata6 in conjunction with reciprocal replacement with a transgene encoding either Gata4 or Gata6, during the pressure overload response. We determined that Gata4 and Gata6 play a redundant and dosage-sensitive role in programming the hypertrophic growth response itself following pressure overload stimulation. However, non-redundant functions were identified as functional decompensation induced by either Gata4 or Gata6 deletion was not rescued by the reciprocal transgene, and only Gata4 heart-specific deletion produced a reduction in capillary density after pressure overload. Gene expression profiling from hearts of these gene-deleted mice showed both overlapping and unique transcriptional codes, with Gata4 exhibiting the strongest impact. These results indicate that Gata4 and Gata6 play a dosage-dependent and semi-redundant role in programming cardiac hypertrophy, but that each has a unique role in maintaining cardiac homeostasis and adaptation to injury that cannot be compensated by the other. Microarray-bassed gene expression profiling identified overlapping, distinct, and quantitatively/differentially regulated classes of Gata4 or Gata6 regulated genes. To determine if Gata4 and Gata6 are redundant or have non-overlapping roles in programming cardiac hypertrophic responses and adaptation to stress or injury, we performed cardiomyocyte-specific conditional gene deletions for Gata4 and Gata6 in conjunction with reciprocal replacement with a transgene encoding either Gata4 or Gata6, during the pressure overload response.

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Skeletal muscle myoblasts: GATA4-Wt, -KO, -OE; day 0, 3

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Comparison of cardiomyocyte transcripts after knockdown of Gata4 in zebrafish embryos

Project description:The Gata4 transcription factor is essential for normal heart development, but the molecular basis for its function remain poorly understood. We profiled at the whole genome level transcript changes in cardiomyocytes when Gata4 is depleted from zebrafish embryos. Our objective was to elucidate the cardiomyocyte-specific molecular program functioning downstream of Gata4 in order to better understand the role of Gata4 in cardiac morphogenesis. Six samples in total are deposited. Three replicate control samples and three replicate Gata4 morphant samples were analyzed.

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2015-04-10 | E-GEOD-67703 | biostudies-arrayexpress

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Genome-wide analysis of gene expression in TM4 Sertoli cells following siRNA-mediated Gata4 inhibition

Project description:The effects of Gata4 inhibition on global gene expression in TM4 Sertoli cells was analyzed. Using microarray analysis we identified a set of genes that are downregulated or upregulated following siRNA-mediated silencing of Gata4 in the murine Leydig tumor cell line mLTC-1. Among the downregulated genes were enzymes of the androgen biosynthetic pathway. TM4 cells were transfected with non-targeting (NT) siRNA and Gata4 siRNA respectively. 72h post transfection cells were lysed and RNA was extracted. n=3 of each sample group; control samples are samples 3-6 (TM4 cells treated with non-targeting siRNA)

2016-03-17 | E-GEOD-74471 | biostudies-arrayexpress

Genome-wide analysis of gene expression in mLTC-1 cells following siRNA-mediated Gata4 inhibition

Project description:The effects of Gata4 inhibition on global gene expression in mLTC-1 cells was analysed. Using microarray analysis we identified a set of genes that are downregulated or upregulated following siRNA-mediated silencing of Gata4 in the murine Leydig tumor cell line mLTC-1. Among the downregulated genes were enzymes of the androgen biosynthetic pathway. mLTC-1 cells were transfected with non-targeting (NT) siRNA and Gata4 siRNA respectively. 72h post transfection cells were lysed and RNA was extracted. n=3 of each sample group; control samples are samples 3-6 (mLTC-1 cells treated with non-targeting siRNA)

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Chromatin immunoprecipitation to identify binding sites for Gata4, Mef2a, Nkx2.5, Srf, p300, Pol_II, H3ac, H3K4me1 in mouse cardiomyocyte cell line, HL1

Project description:The aim of the experiment was to identify genome wide binding sites for Gata4, Mef2a, Nkx2.5, Srf, p300, Pol_II, H3ac, H3K4me1 by using Chromatin Immunoprecipitation followed by microarray analysis (ChIP-chip) in HL1 cells.

2011-01-05 | E-TABM-378 | biostudies-arrayexpress

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