Mus musculus
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ABSTRACT:
PROVIDER: PRJNA148711 | ENA |
REPOSITORIES: ENA
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Project description:Analysis of the transcriptome of cardiac tissue from mice transgenically expressing human cardiolipin synthesis. The hypothesis tested was that cardiac specific transgenic expression of cardiolipin synthase alters myocardial lipidomic flux resulting in compensatory metabolic gene transcriptional changes that will attenuate pathological environmental and dietary insults on bioenergetics. Total RNA obtained from cardiac tissue from transgenic cardiac specific expressing human cardiolipin synthase 1 (hCLS1) mouse model at 4 months of age compared to wildtype littermates
2011-11-05 | E-GEOD-33451 | biostudies-arrayexpress
Project description:Analysis of the transcriptome of cardiac tissue from mice transgenically expressing human cardiolipin synthesis. The hypothesis tested was that cardiac specific transgenic expression of cardiolipin synthase alters myocardial lipidomic flux resulting in compensatory metabolic gene transcriptional changes that will attenuate pathological environmental and dietary insults on bioenergetics.
2011-11-05 | GSE33451 | GEO
Project description:The fatty acid synthase (FASN) is the major fat synthesizing enzyme. FASN is an indispensable enzyme because mice with genetic deletion of Fasn are not viable. Apart from its physiological function, previous studies indicated that FASN could also exert a pathophysiological role, in the heart, because patients with heart failure showed up-reguation of FASN. To investigate the in vivo function of FASN up-regulation in the heart, we generated mice with myocardium-specific expression of FASN under control of the alpha-MHC promoter. Two different founder lines were generated with high and low FASN over-expression. Microarray gene expression profiling of heart tissue was performed of heart tissue from transgenic mice with high and low FASN expression Microarray gene expression profiling was performed with heart tissue isolated from three study groups: (i) Transgenic mice with high cardiac FASN expression, (ii) transgenic mice with low cardiac FASN expression, and (iii) B6 control mice.
2013-07-31 | E-GEOD-49351 | biostudies-arrayexpress
Project description:The atrioventricular (AV) node is a recurrent source of potentially life-threatening arrhythmias. Nevertheless, limited data are available on its developmental control or molecular phenotype. We used a novel AV node-specific reporter mouse to gain insight into the gene programs determining the formation and phenotype of the AV node. In the transgenic reporter, green fluorescent protein (GFP) expression was driven by 160 kbp of Tbx3 and flanking sequences. GFP was selectively expressed in the AV canal of embryos, and in the AV node of adults, while all other Tbx3+ conduction system components, including the AV bundle, were devoid of GFP expression. Fluorescent AV nodal (Tbx3BAC-Egfp) and complementary working (NppaBAC336-Egfp) myocardial cell populations of E10.5 embryos and E17.5 fetuses were purified using fluorescence-activated cell sorting, and their expression profiles were assessed by microarray analysis. We constructed a comprehensive list of sodium, calcium, and potassium channels specific for the nodal or working myocard. Furthermore, the data revealed that the AV node and the working myocardium phenotypes diverge during development, but that the functional gene classes characteristic for both compartments are maintained. Interestingly, the AV node-specific gene repertoire consisted of multiple neurotrophic factors not yet appreciated to play a role in nodal development. These data present the first genome-wide transcription profiles of the AV node during development, providing valuable information concerning its molecular identity. Keywords: Tbx3, AV node, working myocardium, embryonic development, cardiac development, cardiac conduction system 24 samples: 6x working myocardium stage E10.5 (NppaBAC336-Egfp mice), 6x AV canal myocardium stage E10.5 (Tbx3BAC-Egfp mice), 6x working myocardium stage E17.5 (NppaBAC336-Egfp mice), 6x AV node myocardium stage E17.5 (Tbx3BAC-Egfp mice)
2009-06-02 | E-GEOD-13614 | biostudies-arrayexpress
Project description:The cellular and molecular aspects of post-infarct left-ventricle remodeling in presence of type-2 diabetes is poorly understood. In this study we have addressed the cellular and molecular aspects underlying post-infarct left-ventricle remodeling in type 2 diabetic (T2DM) mice using genome-wide mRNA-sequencing. Myocardial infarction was induced by ligating left-anterior descending artery (LAD) in 12-14 month old T2DM and control mice. Cardiac MRI was performed at baseline, day 7 and 14 post-LAD ligation. Blood and tissue samples were collected for biochemical and immunohistochemical, molecular biology analysis after sacrification at day 7 and 14. Genome-wide mRNA sequencing analysis was performed from left-ventricular tissues collected at day 7 post-LAD ligation. Mitochondrial dynamics, Leukocyte recruitment and Collagen I deposition were analyzed using electron microscopy, fluorescent assisted cell sorting (FACS) and fourier-transform infra-red (FTIR) spectroscopy from left ventricular tissues collected at day 7 and 14 post-LAD ligation. Cardiac ejection fraction (EF) and stroke volume (SV) were significantly reduced along with increased mortality in T2DM compared to controls. Ingenuity pathway analyses of differentially expressed genes were enriched for mitochondrial dysfunction, TCA cycle and fatty acid oxidation. Additionally, upstream transcription factor analysis showed inhibition of PGC1a, PGC1b, ESRRA, ESRRB and TFAM in infarcted myocardium of T2DM mice. Electron microscopy analysis showed an altered mitochondrial dynamics and cardiomyocyte death in ischemic myocardium of T2DM mice. Leukocytes exhibited an altered phenotype in ischemic myocardium of T2DM mice. Neovascularization was impaired and collagen deposition was increased in ischemic myocardium of T2DM mice. We conclude that an altered mitochondrial dynamics, cell death modalities, leukocyte phenotype, neovascularization responses and fibrosis may contribute to an increased mortality after myocardial infarction in T2DM. Modulation of mitochondrial dynamics and cardiomyocyte cell death modalities may offer a novel therapeutic target.
2017-11-08 | GSE69201 | GEO
Project description:Here we show that synthesis of the mitochondrial phospholipid cardiolipin is an indispensable driver of thermogenic fat function. Cardiolipin biosynthesis is robustly induced in brown and beige adipose upon cold exposure. Mimicking this response by overexpressing cardiolipin synthase (Crls1) enhances energy consumption in mouse and human adipocytes. Crls1 deficiency diminishes mitochondrial uncoupling in brown and beige adipocytes and elicits a nuclear transcriptional response through ER stress-mediated retrograde communication. Cardiolipin depletion in brown and beige fat abolishes adipose thermogenesis and glucose uptake and renders animals strikingly insulin resistant. We further identify a rare human CRLS1 variant associated with insulin resistance and show that adipose CRLS1 levels positively correlate with insulin sensitivity. Thus, adipose cardiolipin is a powerful regulator of organismal energy homeostasis through thermogenic fat bioenergetics.
2018-07-19 | GSE110297 | GEO
Project description:Analysis of the transcriptome of cardiac tissue from mice trangenically engineered with a doxycycline inducible Tafazzin shRNA knockdown to mimic the loss of function of Tafazzin in Barth syndrome. ShRNA induced knockdown mice were compared to wildtype littermates also fed the doxycyline diet. The hypothesis was to investigate adaptive metabolic and compensatory gene transcriptional changes in myocardium of the mouse model of Barth syndrome Total RNA obtained from 2 month old cardiac tissue from the doxycycline inducible shRNA Tafazzin knockdown mouse model of Barth syndrome compared to wildtype littermates also fed 625 mg/Kg doxycycline diet
2011-11-05 | E-GEOD-33452 | biostudies-arrayexpress
Project description:To describe the transcriptional changes associated with polymicrobial-sepsis induced myocardial depression in wild type and iNOS deficient mice. Keywords: myocardium, contractility, differential gene expression, nitric oxide synthase, infection
2010-11-17 | GSE9667 | GEO
Project description:Mice lacking the zinc finger transcription factor Specificity protein 3 (Sp3) die prenatally in the C57Bl/6 background. To elucidate the cause of mortality we analyzed the potential role of Sp3 in embryonic heart development. Sp3 null hearts display defective looping at E10.5, and at E14.5 the Sp3 null mutants have developed a range of severe cardiac malformations. In an attempt to position Sp3 in the cardiac developmental hierarchy, we analysed the expression patterns of >15 marker genes in Sp3 null hearts. Expression of Cardiac ankyrin repeat protein (Carp) was downregulated prematurely after E12.5, while expression of the other marker genes was not affected. ChIP analysis revealed that Sp3 is bound to the Carp promoter region in vivo. Microarray analysis indicates that small molecule metabolism and cell-cell interactions are the most significantly affected biological processes in E12.5 Sp3 null myocardium. Since the epicardium showed distension from the myocardium, we studied expression of Wt1, a marker for epicardial cells. Wt1 expression was diminished in epicardium-derived cells in the myocardium of Sp3 null hearts. We conclude that Sp3 is required for normal cardiac development, and suggest that it has a crucial role in myocardial differentiation. ( Keywords: Transcription factors, Sp3, knockout mice, cardiac malformations, E12.5
2007-11-01 | GSE9124 | GEO
Project description:Transcriptome analysis of RNA samples from cultured cardiac fibroblasts Excessive extracellular matrix accumulation in the myocardium is a poor prognostic factor for reduced left ventricular function. It is known that improvement of hemodynamic loading improves myocardial fibrosis, but in vitro models of the pathogenesis have not been established, and the potential mechanism of fibrosis resolution have not clarified. We reproduced normal myocardium, fibrotic myocardium following hemodynamic loading and myocardium with improved fibrosis following hemodynamic loading reduction in vitro. Fibroblasts were activated to αSMA+ fibroblasts on myocardium following hemodynamic loading. On myocardium following hemodynamic loading reduction, they were deactivated to αSMA- fibroblasts, and their phenotype changed to fibrinolytic cells expressing MMP2 and MMP9. Comprehensive gene expression analysis of fibroblasts in each in vitro model revealed that Selenbp1 is one of the genes responsible for regulation of phenotypic changes in fibroblasts. In vitro, knockdown of Selenbp1 using RNA interference enhanced fibroblast activation and inhibited conversion to the fibrinolytic form. In vivo, knockdown of Selenbp1 caused structural changes in the left ventricle associated with progressive tissue fibrosis and left ventricular diastolic failure. Selenbp1 is involved in the regulation of fibroblast phenotype and was found to be one of the major molecules regulating collagen turnover in cardiac fibrosis.
2025-10-03 | GSE214665 | GEO