Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA283911 | ENA |
REPOSITORIES: ENA
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Project description:Transcriptional effects of CTGF inhibition in a transgenic mouse model of dilated cardiomyopathy
| PRJNA283911 | ENA
Project description:Cardiac structural changes associated with dilated cardiomyopathy (DCM) include cardiomyocyte hypertrophy and myocardial fibrosis. Connective Tissue Growth Factor (CTGF) has been associated with tissue remodeling and is highly expressed in failing hearts. To test if inhibition of CTGF would alter the course of cardiac remodeling and preserve cardiac function in the protein kinase Cε (PKCε) mouse model of DCM. Transgenic mice expressing constitutively active PKCε in cardiomyocytes develop cardiac dysfunction that was evident by 3 months of age, and that progressed to heart failure, cardiac fibrosis, and increased mortality. Beginning at 3 months of age, mice were treated with an antibody to CTGF (FG-3149) or non-immune IgG control antibody for an additional 3 months. CTGF inhibition significantly improved left ventricular (LV) systolic and diastolic function in PKCε mice, and slowed the progression of LV dilatation. Using gene arrays and quantitative PCR, the expression of many genes associated with tissue remodeling were elevated in PKCε mice, but significantly decreased by CTGF inhibition, however total collagen deposition was not attenuated. The observation of significantly improved LV function by CTGF inhibition in PKCε mice suggests that CTGF inhibition may benefit patients with DCM. Total RNA was isolated from the left ventricle of 6-month-old PKCε transgenic mice or nontransgenic FVB/N controls 3 months after initiation of treatment with IgG (n=10 biological replicates each) or anti-CTGF antibody FG-3149 (n=12 each) and hybridized to Affymetrix 430A 2.0 microarrays. CEL files were processed by GCRMA and rescaled using median per-gene normalization in GeneSpring GX 7.3.1.
2015-11-20 | E-GEOD-68857 | biostudies-arrayexpress
Project description:Cardiac structural changes associated with dilated cardiomyopathy (DCM) include cardiomyocyte hypertrophy and myocardial fibrosis. Connective Tissue Growth Factor (CTGF) has been associated with tissue remodeling and is highly expressed in failing hearts. To test if inhibition of CTGF would alter the course of cardiac remodeling and preserve cardiac function in the protein kinase Cε (PKCε) mouse model of DCM. Transgenic mice expressing constitutively active PKCε in cardiomyocytes develop cardiac dysfunction that was evident by 3 months of age, and that progressed to heart failure, cardiac fibrosis, and increased mortality. Beginning at 3 months of age, mice were treated with an antibody to CTGF (FG-3149) or non-immune IgG control antibody for an additional 3 months. CTGF inhibition significantly improved left ventricular (LV) systolic and diastolic function in PKCε mice, and slowed the progression of LV dilatation. Using gene arrays and quantitative PCR, the expression of many genes associated with tissue remodeling were elevated in PKCε mice, but significantly decreased by CTGF inhibition, however total collagen deposition was not attenuated. The observation of significantly improved LV function by CTGF inhibition in PKCε mice suggests that CTGF inhibition may benefit patients with DCM.
2015-11-20 | GSE68857 | GEO
Project description:Transcriptional effects of CTGF inhibition and gemcitabine in the KPC mouse model of pancreatic ductal adenocarcinoma
| PRJNA198031 | ENA
Project description:Gene expression profiling of a mouse model of dilated cardiomyopathy
| PRJNA117695 | ENA
Project description:Gene expression profiling in homozygous LMNA-/- mouse model with cardiomyopathy phenotype unraveled novel LMNA-mediated alterations of signaling pathways leading to dilated cardiomyopathy
2020-04-27 | GSE133693 | GEO
Project description:Changes in the gene expression in the heart of knock-in mouse model of dilated cardiomyopathy caused by delK210 mutation in cardiac troponin T.
2008-09-04 | E-MEXP-1340 | biostudies-arrayexpress
Project description:Truncating variants in titin can cause dilated cardiomyopathy, however, the role of missense titin variants is less clear. In humans the heterozygous titin A178D variant is associated with dilated cardiomyopathy with left ventricular non-compaction. Using CRISPR-Cas9 mediated homology-directed repair the A178D titin variant was introduced into a mouse model. Homozygous A178D mice showed features of dilated cardiomyopathy. Total RNA was extracted from the left ventricles of WT and homozygous A178D littermate control mice and RNA-sequencing performed. Different patterns of gene expression were identified in wildtype and homozygous A178D left ventricles.
2021-02-26 | GSE154504 | GEO
Project description:This experiment aimed to investigate the transcriptional role of G4 resolvase Dhx36 in the adult mouse heart. We compared three pools of wild-type (WT) mouse hearts with three pools of Dhx36 conditional knockout (cKO) hearts. In the mutant mice, Dhx36 was conditionally deleted in cardiomyocytes using the Myh6-cre transgenic line. Each of the six pools was created using RNA extracted from 3-5 hearts from mice aged approximately 21 days. The cKO mice developed dilated cardiomyopathy and began experiencing sudden death at 40 days old, with no mutants surviving beyond 5 months.
2024-09-15 | E-MTAB-14440 | biostudies-arrayexpress
Project description:Gene expression profiling on mouse models of dilated cardiomyopathy
| PRJNA99861 | ENA