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Heart failure in TNF-alpha transgenic mice

ABSTRACT: Cardiac-specific TNF-alpha transgenic mice are an excellent model to study the pathologenesis of heart failure. Affymetrix U74V2A was used to analyze the gene expression profile of male and female wildtype FVB and TNF-alpha transgenic mice at the time point of compensated hypertrophy and dilated heart failure. 3 week, 13 week and 40 week samples examined. Keywords: other

ORGANISM(S): Mus musculus

PROVIDER: GSE591 | GEO | 2003/11/09

SECONDARY ACCESSION(S): PRJNA85377

REPOSITORIES: GEO

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Transcription profiling of male and female wildtype FVB and TNF-alpha transgenic mice at the time point of compensated hypertrophy and dilated heart failure to study the molecular mechanism of heart failure.

Project description:Cardiac-specific TNF-alpha transgenic mice are an excellent model to study the pathologenesis of heart failure. Affymetrix U74V2A was used to analyze the gene expression profile of male and female wildtype FVB and TNF-alpha transgenic mice at the time point of compensated hypertrophy and dilated heart failure. 3 week, 13 week and 40 week samples examined.

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Gene expression profiling of cardiac-specific overexpression of TNF-α in Des-/- myocardium

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Project description:We have used chronic cardiac pacing in conscious dogs to study mechanism related to the development of dilated cardiomyopathy and the transition from compensated dysfunction (CD) to decompensated heart failure (HF). This occurs from the 3rd to 4th week of pacing with end-stage HF at 30?1 days. Keywords: disease state analysis

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Project description:The study applied NGS to determine the cardiac transcriptomes of BBLN-transgenic mice with FVB/N background in comparison to those of non-transgenic FVB/N mice at an age of 8 months. The BBLN (Bublin coiled-coil protein) is the chromosome 9 open reading frame, C9orf16, with largely unknown function. To investigate the cardiac phenotype of increased cardiac BBLN transcript levels we generated BBLN-transgenic (Tg-BBLN) mice. Echocardiography documented that Tg-BBLN mice developed features of heart failure at an age of 8 months. To elucidate pathomechanisms of heart failure induced by BBLN, we performed NGS of the cardiac transcriptomes of eight-month-old, male, BBLN-transgenic mice with cardiac-specific expression of BBLN under control of the myocardium-specific, alpha-MHC promoter. The non-transgenic control group are age-matched, male, nontransgenic FVB/N mice. NGS data of this study document transcriptome changes underlying the heart failure phenotype induced by transgenic BBLN expression.

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Project description:The RAF kinase inhibitor protein, RKIP, is a dual inhibitor of the RAF1 kinase and the G-protein-coupled receptor kinase 2 (GRK2). By inhibition of the proto-oncogenic and pro-survival RAF1-MAPK pathway, the RAF kinase inhibitor protein, RKIP, acts as a tumor suppressor, which enhances cardiomyocyte death and promotes the development of symptoms of heart failure. To elucidate pathomechanisms of heart failure induced by RKIP, the study determined the cardiac transcriptomes of eight-month-old, male, transgenic mice with cardiac-specific expression of RKIP (PEBP1) under control of the myocardium-specific, alpha-MHC promoter. In addition, the study determined the cardiac transcriptomes of GRK2-transgenic mice. Tg-GRK2 mice have a slightly increased transgenic expression of GRK2. According to NGS data, cardiac GRK2-Grk2 transcript levels of Tg-GRK2 mice are 1.59±0.10-fold higher than those of non-transgenic FVB hearts. In Tg-GRK2 mice, transgenic GRK2 is expressed under control of the ubiquitous CMV immediate-early promoter/enhancer. The non-transgenic control group are age-matched, male, nontransgenic FVB/N mice. NGS data of this study document transcriptome changes underlying the heart failure phenotype induced by transgenic RKIP expression and cardiac degeneration induced by GRK2 expression.

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Project description:Agonist-induced cardiac hypertrophy in TG1306/1R transgenic mice with cardiac angiotensin II overproduction leads to a gradual transition from a compensatory hypertrophic state to heart failure. To gain insight into the molecular mechanisms that play a role in maintaining cardiac integrity in the diseased heart, we performed a comparative study of gene expression between wild-type (WT) and transgenic (TG) hearts using microarray analysis. TG1306/1R transgenics were separated into two phenotypic groups (hypertrophic and dilated) based on morphological parameters (cardiac weight index and histology) and either a moderate (hypertrophic) or a high (dilated) upregulation of molecular markers for hypertrophy and failure, and compared to age and sex-matched wild-types. In this series, twelve 60 week old male TG1306/1R mice were separated into 3 groups: WT1-4= Four Wild-types TG1306/1R littermates genetically negative for the transgene (-/-) Hyp1-4= Four TG1306/1R mice heterozygote for the transgene (-/+) and developing a concentric hypertrophic phenotype* Dil1-4 = Four TG1306/1R mice heterozygote for the transgene (-/+) and developing a dilated cardiac phenotype* This series contains 4 biological replicates for the following triangulation: WT is compared to Hyp, WT is compared to Dil, and Hyp is compared to Dil. * For further information read: Domenighetti AA, Wang Q, Egger M, Richards SM, Pedrazzini T, Delbridge LM. Angiotensin II-mediated phenotypic cardiomyocyte remodeling leads to age-dependent cardiac dysfunction and failure. Hypertension. 2005 Aug;46(2):426-32. [PMID: 15998712]

2010-05-18 | E-GEOD-13336 | biostudies-arrayexpress

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2018-06-06 | PXD008934 | Pride

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