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E-GEOD-3866

ABSTRACT: Transcription profiling by array of left ventricle tissues from rat with overexpression of constitutively active upstream kinase mitogen-activated protein kinase kinase 3b (MKK3bE) and wild-type p38? in the heart

OTHER RELATED OMICS DATASETS IN: PRJNA94101

PROVIDER: E-GEOD-3866 | ExpressionAtlas | 2014-10-10

REPOSITORIES: ExpressionAtlas

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			Action	DRS
	E-GEOD-3866-analysis-methods.tsv	Tabular
	E-GEOD-3866-atlasExperimentSummary.Rdata	Rdata
	E-GEOD-3866-configuration.xml	Xml
	E-GEOD-3866-percentile-ranks.tsv	Tabular
	E-GEOD-3866.condensed-sdrf.tsv	Tabular

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Transcription profiling by array of left ventricle tissues from rat with overexpression of constitutively active upstream kinase mitogen-activated protein kinase kinase 3b (MKK3bE) and wild-type p38? in the heart

Project description:Mitogen-activated protein kinases (MAPKs) regulate cardiomyocyte growth and apoptosis in response to extracellular stimulation, but the downstream effectors that mediate their pathophysiological effects remain poorly understood. We determined the targets and role of p38 MAPK in the heart in vivo by using local adenovirus-mediated gene transfer of constitutively active upstream kinase mitogen-activated protein kinase kinase 3b (MKK3bE) and wild-type p38Î± in rats. DNA microarray analysis of animals with cardiac-specific overexpression of p38 MAPK revealed that 264 genes were upregulated more than 2-fold including multiple genes controlling cell division, cell signaling, inflammation, adhesion and transcription. Several previously unknown p38 target genes were found. Using gel mobility shift assays we identified several cardiac transcription factors that were directly activated by p38 MAPK. Finally, we determined the functional significance of the altered cardiac gene expression profile by histological analysis and echocardiographic measurements, which indicated that p38 MAPK overexpression induced gene expression results in cell proliferation, myocardial inflammation and fibrosis. In conclusion, we defined the novel target genes and transcription factors as well as the functional effects of p38 MAPK in the heart. Expression profiling of p38 MAPK overexpression identified cell cycle regulatory and inflammatory genes critical for pathological processes in the adult heart. Experiment Overall Design: Left ventricular gene expression profiles three days after MKK3bE + WT p38Î± gene transfer were compared with those of Lac Z âtreated animals by screening Affymetrix Rat Expression Set 230_2.0 Arrays (there are 5 samples in both group).

2009-04-25 | E-GEOD-3866 | biostudies-arrayexpress

p38 MAPK overexpression in heart in vivo.

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