Expression analysis of transgenic mice with a cardiac specific overexpression of DSC2.
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
SUBMITTER: Andreas Brodehl
PROVIDER: E-GEOD-84645 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:Gene expression data indicate an early up-regulation of inflammatory and fibrotic remodeling pathways in DSC2 transgenic mice vs. non-transgenic control mice. The mice were analyzed at the age of 3.5 and 13 weeks. The mice were analyzed at the age of 3.5 and 13 weeks.
2016-07-21 | GSE84645 | GEO
Project description:The anti-diabetic drug and agonist of the peroxisome proliferator-activated receptor gamma (Pparg), rosiglitazone, was recently withdrawn in many countries because the drug use was associated with an increased risk of heart failure. To investigate underlying pathomechanisms, we chose 6-month-old apolipoprotein E (apoE)-deficient mice, which are prone to atherosclerosis and insulin resistance, and thereby mimic the risk profile of patients with cardiovascular disease. After 8 weeks of rosiglitazone treatment (30 mg/kg/day), echocardiography and histology analyses demonstrated that rosiglitazone had induced heart failure with cardiac dilation. Concomitantly, cardiac lipid overload and lipid-induced cardiomyocyte death developed. The microarray gene expression study of heart tissue from rosiglitazone-treated apoE-deficient mice relative to untreated apoE-deficient mice and non-transgenic B6 mice identified cardiac Pparg-dependent lipid metabolism genes in rosiglitazone-treated mice, which seem to trigger a major heart failure promoting pathway. Microarray gene expression profiling was performed with heart tissue isolated from three study groups: (i) rosiglitazone-treated 8-month-old apolipoprotein (apoE)-deficient mice with symptoms of heart failure, (ii) untreated 8-month-old apoE-deficient mice, and (iii) age-matched, untreated, non-transgenic B6 control mice.
2011-03-18 | E-GEOD-28031 | biostudies-arrayexpress
Project description:Depletion of cardiac ATP content is a characteristic feature of heart failure in patients and experimental animal models. To analyze the impact of insufficient ATP supply on heart function we inhibited cellular respiration by disulfide poisoning with the mild thiol-blocking agent, cystamine. We chose 4 month-old apolipoprotein E (apoE)-deficient mice, which are highly vulnerable to increased oxygen and ATP demands. After 4 weeks of cystamine treatment (300 mg/kg in drinking water), echocardiography and histology analyses demonstrated that apoE-deficient mice had developed heart failure with cardiac dilation. The microarray gene expression study of heart tissue from cystamine-treated apoE-deficient mice relative to untreated mice confirmed the development of heart failure showing up-regulation heart failure-specific genes by mild thiol-blocking with cystamine. Microarray gene expression profiling was performed with heart tissue isolated from three study groups: (i) cystamine-treated 5 month-old apolipoprotein- (apoE)- deficient mice with symptoms of heart failure, (ii) untreated 5 month-old apoE- deficient mice, and (iii) age-matched, untreated, non-transgenic B6 control mice.
2010-12-03 | E-GEOD-25768 | biostudies-arrayexpress
Project description:We harvested the heart from transgenic mice with cardiac specific overexpression of Sirt1 (Tg-Sirt1) and non-transgenic (NTg) control littermate at 3 months of age and then microarray analyses were conducted. Experiment Overall Design: Two transgenic mice and two wild type mice were used.
2008-06-15 | E-GEOD-7407 | biostudies-arrayexpress
Project description:Atherosclerosis and pressure overload are major risk factors for the development of heart failure in patients. Cardiac hypertrophy often precedes the development of heart failure. However, underlying mechanisms are incompletely understood. To investigate pathomechanisms underlying the transition from cardiac hypertrophy to heart failure we used experimental models of atherosclerosis- and pressure overload-induced cardiac hypertrophy and failure, i.e. apolipoprotein E (apoE)-deficient mice, which develop heart failure at an age of 18 months, and non-transgenic C57BL/6J (B6) mice with heart failure triggered by 6 months of pressure overload induced by abdominal aortic constriction (AAC). The development of heart failure was monitored by echocardiography, invasive hemodynamics and histology. The microarray gene expression study of cardiac genes was performed with heart tissue from failing hearts relative to hypertrophic and healthy heart tissue, respectively. The microarray study revealed that the onset of heart failure was accompanied by a strong up-regulation of cardiac lipid metabolism genes involved in fat synthesis, storage and oxidation. Microarray gene expression profiling was performed with heart tissue isolated from (i) 18 month-old apoE-deficient mice relative to age-matched non-transgenic C57BL/6J (B6) mice, (ii) 6 month-old apoE-deficient mice with 2 months of chronic pressure overload induced by abdominal aortic constriction (AAC) relative to sham-operated apoE-deficient mice and nontransgenic B6 mice, (iii) 10 month-old B6 mice with 6 months of AAC relative to sham-operated B6 mice, and (iv) 5 month-old B6 mice with 1 month of AAC relative to age-matched B6 mice.
2010-12-03 | E-GEOD-25765 | biostudies-arrayexpress
Project description:CUG-BP, Elav-like family (CELF) proteins regulate alternative splicing. In MHC-CELFdelta transgenic mice, CELF-mediated alternative splicing is disrupted in heart muscle via expression of a nuclear dominant negative CELF protein under an alpha-myosin heavy chain promoter. MHC-CELFdelta mice develop dilated cardiomyopathy and contractile dysfunction by 3 weeks of age, shortly after the transgene is activated and splicing defects appear. Cardiac function and heart size spontaneously recover with age in a low-expressing (mild) line of MHC-CELFdelta mice despite persistence of dominant negative protein expression and splicing defects, whereas there is no recovery in a higher-expressing (severe) line that also experiences early muscle death and fibrosis. In this study, we explored the basis for this functional recovery by comparing the gene expression profiles in the hearts of low- and high-expressing lines of MHC-CELFdelta mice to those of wild type littermates at 3 weeks (when cardiac dysfunction is maximal) and 24 weeks (when the low-expressing line has recovered) using microarrays. We found that differences in gene expression are greatly reduced in older animals from the low-expressing line, but were exacerbated in the high-expressing line. We did not find evidence of a new compensatory pathway being activated in the low-expressing line with age, and propose that recovery may occur due to developmental stage-specific compatibility of CELF-dependent splice variants with the changing cellular environment of cardiomyocytes. Microarray analysis was performed on total RNA extracted from whole hearts of female mice: three MHC-CELFdelta-10 (high-expressing line) and three MHC-CELFdelta-574 (low-expressing line) were collected at 3 weeks, and five MHC-CELFdelta-10 and five MHC-CELFdelta-574 were collected at 24 weeks. Two wild type mice from each line were collected at each time point (n = 4 total wild type at 3 weeks, and n = 4 total wild type at 24 weeks).
2014-10-16 | E-GEOD-62363 | biostudies-arrayexpress
Project description:To identify the gene expression changes that are specific to SBMA, we prepared total mRNA samples from the spinal cords of transgenic mice carrying a full-length human AR with 97 CAGs (AR-97Q), transgenic mice bearing a wild-type allele of AR with 24 CAGs (AR-24Q), and the wild-type littermates of the AR-97Q mice (C57BL/6). We used AR-97Q (Line #7-8) male mice because they show progressive muscular atrophy and weakness as well as SBMA-like pathology such as the accumulation of the pathogenic androgen receptor in the nucleus of motor neurons. Using microarray analysis, we identified the genes with significantly altered expression among the three types of mice. For each group, we examined the male mice at 7-9, 10-12, and 13-15 weeks of age. These stages were chosen because the AR-97Q mice are generally asymptomatic at 7-9 weeks of age (before-onset stage), present with mild motor impairment at 10-12 weeks (early stage), and are severely weakened with profound muscle atrophy at 13-15 weeks (advanced stage). RNA from the total spinal cord, excluding the dorsal root ganglia, was isolated from three mice of each genotype at each stage. For wild-type, pooled sample for three mice were used in each stage.
2012-08-03 | E-GEOD-39865 | biostudies-arrayexpress
Project description:Seven male C57BL/6 mice, at 10 weeks of age, were injected daily intraperitoneally with 0.5 mg/kg of haloperidol, for 28 days. A control group of six animals was injected with vehicle only (saline).
2015-11-30 | PXD002250 | Pride
Project description:Specific pathogen free wild-type C57Bl/6 male mice fed ketogenic diet (Bio-Serv AIN-76-A) for 4 weeks Keywords: RNA Expression Array Hearts from 12 week-old mice that were maintained on a standard polysacchardide-rich chow until the age of 8 weeks, at which time they were switched to a ketogenic diet (ad libitum) and maintained for 4 additional weeks prior to collection of tissues
2010-06-16 | E-GEOD-21368 | biostudies-arrayexpress
Project description:Heart failure is a leading cause of cardiovascular mortality with limited options for treatment. We used 18 month-old apolipoprotein E (apoE)- deficient mice as a model of atherosclerosis-induced heart failure to analyze whether the anti-ischemic drug ranolazine could retard the progression of heart failure. The study showed that 2 months of ranolazine treatment improved cardiac function of 18 month-old apoE-deficient mice with symptoms of heart failure as assessed by echocardiography. To identify changes in cardiac gene expression induced by treatment with ranolazine a microarray study was performed with heart tissue from failing hearts relative to ranolazine-treated and healthy control hearts. The microarray approach identified heart failure-specific genes that were normalized during treatment with the anti-ischemic drug ranolazine. Microarray gene expression profiling was performed with heart tissue isolated from (i) untreated 18 month-old apoE-deficient mice with heart failure relative to (ii) 18 month-old apoE-deficient mice treated for two months with the anti-ischemic drug ranolazine (200 mg/kg), and (iii) age-matched non-transgenic C57BL/6J (B6) control mice.
2010-12-03 | E-GEOD-25767 | biostudies-arrayexpress