Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA146617 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:The expression of the small molecular weight heat shock protein (Hsp) H11 kinase/Hsp22 (Hsp22) is restricted to a limited number of tissues, including the heart and skeletal muscle, both in rodents and in humans. We generated a mouse knockout (KO) model, and investigated the role of Hsp22 in regulating cardiac hypertrophy in response to pressure overload. We compared gene expression profiles between WT and KO mice in basal condition and three days pressure overload after transverse aortic constriction (TAC). These data illustrated a novel mechanism of Hsp22-related gene expression in response to cardiac stress. We used microarray to examine differential gene expression by Hsp22 deletion at baseline and 3-day pressure overload. Left ventricles from wild type and Hsp22 knockout mice were selected from basal condition (each, n=3) and TAC surgery (each, n=4).
2010-12-31 | E-GEOD-24489 | biostudies-arrayexpress
Project description:The expression of the small molecular weight heat shock protein (Hsp) H11 kinase/Hsp22 (Hsp22) is restricted to a limited number of tissues, including the heart and skeletal muscle, both in rodents and in humans. We generated a mouse knockout (KO) model, and investigated the role of Hsp22 in regulating cardiac hypertrophy in response to pressure overload. We compared gene expression profiles between WT and KO mice in basal condition and three days pressure overload after transverse aortic constriction (TAC). These data illustrated a novel mechanism of Hsp22-related gene expression in response to cardiac stress.
2010-12-31 | GSE24489 | GEO
Project description:Backgound: Cardiac pressure overload, for example in patients with aortic stenosis, induces irreversible damage in the myocardium leading to cardiac dysfunction, cardiomyocyte hypertrophy and interstitial fibrosis. We therefore hypothesized that insufficient cardiac regeneration might contribute to the progression of pressure overload dependent disease. Here, we aimed to elucidate whether pressure overload in the regenerative stage shortly after birth could lead to a more adaptive cardiac response than in the non-regenerative stage in mice.nTAC in the non-regenerative stage induced cardiac dysfunction, myocardial fibrosis and cardiomyocyte hypertrophy. In contrast, during induction of nTAC in the regenerative stage, cardiac function remained intact and this was associated with enhanced myocardial angiogenesis and innervation as well as increased cardiomyocyte proliferation, but neither hypertrophy nor fibrosis. Mechanistically, inhibition of cardiomyocyte proliferation and angiogenesis in nTAC in the regenerative phase by rapamycin triggered mortality and myocardial fibrosis, which both also similarly occurred upon inhibition of angiogenesis by PTK787, suggesting that both processes are essential for the adaptive cardiac response to nTAC. A comparative genome-wide transcriptomic analysis between hearts after nTAC in the regenerative versus the non-regenerative stage defined differentially expressed functional gene classes, and a related bioinformatics analysis suggested the transcription factor GATA4 as master regulator of the regenerative gene-program. Indeed, cardiomyocyte specific deletion of GATA4 converted the regenerative nTAC into a non-regenerative, maladaptive response.tablished a new model of neonatal pressure-overload in mice, which when applied in the regenerative postnatal stage, triggers a purely adaptive myocardial response. Employing this model to identify new regulators might lead to novel therapeutic strategies to combat pressure overload induced myocardial disease.
2019-07-26 | GSE121308 | GEO
Project description:Chronic Benzene Exposure Aggravates Pressure Overload-Induced Cardiac Dysfunction
| PRJNA792555 | ENA
Project description:Left ventricular myocardial transcriptomic profiling was performed in rats subjected to transverse aortic constriction (TAC)-induced heart failure and sham-operated controls to investigate gene expression changes associated with pressure overload-induced cardiac remodeling. The dataset was used in studies investigating novel molecular targets in heart failure, including G-protein-coupled receptor (GPCR)-associated pathways and microRNA-regulated target networks.
2026-06-11 | E-MTAB-17114 | biostudies-arrayexpress
Project description:Myocardial deletion of klf4 sensitizes mouse to pressure overload. In order to gain a better understanding of molecular mechanisms of such alterations, we profiled gene expression before and after 3-day of pressure overload (induced by transverse aortic constriction -TAC) in the hearts from MHC-cre (Cre) control and MHC-cre-klf4-deficient (KO) mice. 10wk old male mice was subjected to transverse aortic constriction (TAC) to induce pressure overload or sham operation as control group. After 3 days, heart was removed and total RNA was extracted from apex and subjected for array analysis. Four animals in each group.
2015-07-01 | E-GEOD-61177 | biostudies-arrayexpress
Project description:The model describes cellular adaptation to proteotoxic stress through four dynamical variables: protein damage, cell survival, molecular chaperone mRNA and molecular chaperone protein. Heat increases the production of misfolded proteins, which are either degraded or repaired by chaperones. Accumulated damage decreases cell survival and also activates chaperone transcription through a negative-feedback mechanism representing HSF1-mediated regulation. The induced increase in chaperone abundance during a first sublethal heat shock can protect cells against a subsequent stress, thereby reproducing thermotolerance and allowing the effects of priming temperature, duration and recovery time to be explored.
2026-09-02 | MODEL2608180005 | BioModels
Project description:Myocardial deletion of klf4 sensitizes mouse to pressure overload. In order to gain a better understanding of molecular mechanisms of such alterations, we profiled gene expression before and after 3-day of pressure overload (induced by transverse aortic constriction -TAC) in the hearts from MHC-cre (Cre) control and MHC-cre-klf4-deficient (KO) mice.
2015-07-01 | GSE61177 | GEO
Project description:Proteomics study of the anthracycline-induced cardiotoxicity in in pigs with pre-existing left ventricular (LV) pressure overload. Large White pigs (2-month-old males and females) were used to induce LV pressure overload via supravalvular aortic stenosis (or sham operation). After 4 months, animals were subsequently exposed to low-risk cumulative doses of anthracyclines (doxorubicin, 5 weekly 1 mg/kg intravenous injections) or vehicle. A total of 16 pigs were divided in four groups: (1) healthy controls (no LV overload or anthracyclines), (2) Doxorubicin (Dox, no LV overload but anthracyclines), (3) Banding (LV overload without anthracyclines), and (4) Banding+Doxorubicin (LV overload plus anthracyclines). A high-throughput quantitative proteomic analysis was performed in myocardial tissue.
2026-02-05 | PXD056684 | Pride
Project description:A molecular and bioinformatic pipeline permitting comprehensive analysis and quantification of myocardial miRNA and mRNA expression with next-generation sequencing was developed and the impact of enhanced PI3Kalpha signaling on the myocardial transcriptome signature of pressure overload-induced pathological hypertrophy was explored. miRNA and mRNA-Seq were carried out in four groups of mouse LV samples: WT sham, WT+TAC, caPI3Kalpha sham, caPI3Kalpha+TAC
2013-05-01 | E-GEOD-35350 | biostudies-arrayexpress