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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.

2007-12-15 | E-GEOD-591 | biostudies-arrayexpress

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

Project description:Tumor Necrosis Factor-α is greatly implicated in heart pathophysiology, while it is upregulated in the failing myocardium. A major target in TNF-α-induced heart failure is the muscle specific intermediate filament cytoskeleton, comprised by desmin. We analysed the effect of cardiac-specific overexpression of TNF-α in the Des-/- myocardium, which is a known model of dilated cardiomyopathy. Hearts of 3 months old mice (n=3) of Des-/- and TNFαDes-/- genotypes were used for whole genome microarray hybridization analysis.

2015-05-02 | E-GEOD-56286 | biostudies-arrayexpress

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

2015-05-02 | GSE56286 | GEO

Mus musculus

Project description:Heart failure in TNF-alpha transgenic mice

| PRJNA85377 | ENA

Whole genome microarray gene expression profiling of transgenic mouse hearts with four-fold increased BBLN contents

Project description:The study performed whole genome microarray gene expression profiling of mouse hearts from BBLN-transgenic mice with four-fold increased cardiac BBLN (Bublin coiled coil protein) contents (Tg-BBLN-low) in comparison to non-transgenic FVB hearts. Tg-BBLN-low mice with four-fold increased cardiac BBLN expression under control of the myocardium-specific alpha-MHC promoter developed features of compensated heart failure with increasing age, which was characterized by a significantly reduced left ventricular ejection fraction as determined by echocardiography. To investigate the compensated heart failure phenotype of Tg-BBLN-low mice, whole genome micoarray gene expression profiling was performed. The microarray data show that moderately increased cardiac BBLN levels are sufficient to induce features of pathological cardiac remodeling.

2023-09-18 | GSE241030 | GEO

Altered expression of a limited number of genes contributes to cardiac decompensation during chronic pacing in dogs

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

2006-10-13 | GSE5247 | GEO

Cardiac transcriptome analysis of BBLN-transgenic mice by NGS

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.

2023-09-18 | GSE241161 | GEO

Cardiac transcriptome analysis of RKIP-transgenic and GRK2-transgenic mice by NGS

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.

2021-12-27 | GSE191316 | GEO

Gene expression profiling in cardiac AngII-overexpressing mice (TG1306/1R)

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

Characterization of proteomic changes in human heart failure

Project description:The microtubule (MT) cytoskeleton can provide a mechanical resistance that can impede the motion of contracting cardiomyocytes. Yet a role of the MT network in human heart failure is unexplored. Here we utilize mass spectrometry to characterize changes to the cytoskeleton in human heart failure. Proteomic analysis of left ventricle tissue reveals a consistent upregulation and stabilization of intermediate filaments and MTs in human heart failure. This dataset includes left ventricular (LV) myocardium from 34 human hearts – either non-failing (NF) or failing hearts. NF hearts are subdivided into normal or compensated hypertrophy (cHyp), while failing hearts are subdivided into ischemic cardiomyopathy (ICM), dilated cardiomyopathy (DCM), and hypertrophic cardiomyopathy with preserved or reduced ejection fraction (HCMpEF and HCMrEF, respectively). Further details on patient classification and in vivo parameters on each heart are listed in sample details.txt.

2018-06-06 | PXD008934 | Pride

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