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Transcription profiling of infarcted rats teated with rhNRG-1(recombinant human NRG-1)

ABSTRACT: The ErbB famliy of erceptor tyrosine kinases and their ligands, neuregulins(NRGs), are crtical involved not only in cardiac development but also in the maintenace of structural and functional integrity of the adult heart. rhNRG-1(recombinant human NRG-1) Improves cardiac function and sruvival in models of ischemic, dilated, and viral cardiomyopathy with the ErbB-activation. But the mechanism is still unknown Experiment Overall Design: Three individual samples in each group (vehicle, rhNRG-1 treated or sham operated rats) were hybridized with 9 GeneChipÂ® Rat Genome 230 2.0 Arrays (Affymetrix) separately.A total of 1950 genes (at least a 1.5-fold change in expression level compared with any another groups, all p <0.05),were selected and used as input for hierarchical clustering, a computational method that groups experimental samples according to similarity in patterns of gene expression across a large number of genes.

ORGANISM(S): Rattus norvegicus

SUBMITTER: zensun biology

PROVIDER: E-GEOD-9263 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Infarcted rats teated with rhNRG-1(recombinant human NRG-1)

Project description:The ErbB famliy of erceptor tyrosine kinases and their ligands, neuregulins(NRGs), are crtical involved not only in cardiac development but also in the maintenace of structural and functional integrity of the adult heart. rhNRG-1(recombinant human NRG-1) Improves cardiac function and sruvival in models of ischemic, dilated, and viral cardiomyopathy with the ErbB-activation. But the mechanism is still unknown Keywords: Genechips

2007-10-18 | GSE9263 | GEO

Alteration in Tyrosine Phosphorylation of Cardiac Proteome and EGFR Pathway Contribute to Hypertrophic Cardiomyopathy

Project description:Alterations of serine/threonine phosphorylation of the cardiac proteome are a hallmark of heart failure. However, the contribution of tyrosine phosphorylation (pTyr) to the pathogenesis of cardiac hypertrophy remains unclear. We use global mapping to discover and quantify site-specific pTyr in two cardiac hypertrophic mouse models, i.e., cardiac overexpression of ErbB2 (TgErbB2) and myosin heavy chain R403Q (R403Q-aMyHC Tg), compared to control hearts. From this, there are significant phosphoproteomic alterations in TgErbB2 mice in right ventricular cardiomyopathy, hypertrophic cardiomyopathy (HCM), and dilated cardiomyopathy (DCM) pathways. On the other hand, R403Q-aMyHC Tg mice indicated that the EGFR1 pathway is central for cardiac hypertrophy, along with angiopoietin, ErbB, growth hormone, and chemokine signaling pathways activation. Surprisingly, most myofilament proteins have downregulation of pTyr rather than upregulation. Kinase-substrate enrichment analysis (KSEA) shows a marked downregulation of MAPK pathway activity downstream of k-Ras in TgErbB2 mice and activation of EGFR, focal adhesion, PDGFR, and actin cytoskeleton pathways. In vivo ErbB2 inhibition by AG-825 decreases cardiomyocyte disarray. Serine/threonine and tyrosine phosphoproteome confirms the above-described pathways and the effectiveness of AG-825 treatment. Thus, altered pTyr may play a regulatory role in cardiac hypertrophic models.

2023-03-10 | PXD036506 | Pride

KDM8 epigenetically controls cardiac metabolism to prevent initiation of dilated cardiomyopathy [CUT&Tag]

Project description:Cardiac metabolism is deranged in heart failure, but underlying mechanisms remain unclear. Lysine demethylase 8 (Kdm8) represses gene expression in the embryo and controls metabolism in cancer. However, its function in cardiac homeostasis is unknown. We show that Kdm8 maintains a mitochondrial gene network active by repressing Tbx15 to prevent dilated cardiomyopathy leading to lethal heart failure. Deletion of Kdm8 in mouse cardiomyocytes increased H3K36me2 with activation of Tbx15 and repression of target genes in the NAD+ pathway before dilated cardiomyopathy initiates. Moreover, NAD+ supplementation prevented dilated cardiomyopathy in Kdm8 mutant mice and TBX15 overexpression blunted NAD+-activated cardiomyocyte respiration. Furthermore, KDM8 was downregulated in human hearts affected by dilated cardiomyopathy and higher TBX15 expression defines a subgroup of affected hearts with the strongest downregulation of genes encoding mitochondrial proteins. Thus, KDM8 represses TBX15 to maintain cardiac metabolism. Our results suggest that epigenetic dysregulation of metabolic gene networks initiates myocardium deterioration towards heart failure and could underlie heterogeneity of dilated cardiomyopathy.

2022-12-23 | GSE215793 | GEO

KDM8 epigenetically controls cardiac metabolism to prevent initiation of dilated cardiomyopathy [RNA-seq]

2022-12-23 | GSE215351 | GEO

RNA-seq identifies novel transcript elements and transcript processing in the normal and failing hearts

Project description:Changes in gene expression contribute to the pathogenesis of heart failure. The sequence, expression level, and structure of the human cardiac transcriptome are incompletely described, as are their changes in heart disease. High throughput transcriptome sequencing (RNA-seq) is a quantitative and unbiased approach to measure transcript level and to identify novel transcribed elements or transcript splicing. Here we acquired 975.2 x 106 mapped RNA-seq reads in 15 control and 15 ischemic cardiomyopathy (ICM) hearts, obtained at the time of heart transplantation. We identified over 1000 differentially expressed transcripts, and thousands of novel transcribed elements, some of which were differentially expressed in between control and ICM groups. We found that transcript processing of several cardiac genes was deranged in ICM. For instance, the ratio between specific MYH6 exons was significantly changed in ICM compared to controls, while this type of inter-exon variation was not observed for the adjoining gene MYH7. This RNA-seq study of the human heart failure transcriptome revealed the diversity of transcripts expressed in the human heart and their complex patterns of expression in the diseased heart. Transcriptome profiling (RNA-seq) of 15 control and 15 ischemic cardiomyopathy (ICM) hearts using Illumina GAII and SOLiD

2013-12-19 | E-GEOD-48166 | biostudies-arrayexpress

changes in cardiac transcription profiles brought about by heart failure

Project description:To establish changes in cardiac transcription profiles brought about by heart failure we collected myocardial samples from patients undergoing cardiac transplantation whose failure arises from different etiologies (e.g. idiopathic dilated cardiomyopathy, ischemic cardiomyopathy, alcoholic cardiomyopathy, valvular cardiomyopathy, and hypertrophic cardiomyopathy) and from "normal" organ donors whose hearts cannot be used for transplants. The transcriptional profile of the mRNA in these samples will be measured with gene array technology. Changes in transcriptional profiles can be correlated with the physiologic profile of heart-failure hearts acquired at the time of transplantation. Keywords: other

2004-03-24 | E-GEOD-1145 | biostudies-arrayexpress

Transcription profiling of wild type and delK210 cTnT knock-in mouse heart to study dilated cardiomyopathy

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

Cardiac disruption of SDHAF4-mediated mitochondrial complex II assembly promotes dilated cardiomyopathy

Project description:Succinate dehydrogenase, which is known as mitochondrial complex II, has proven to be a fascinating machinery, attracting renewed and increased interest in its involvement in human diseases. Herein, we find that succinate dehydrogenase assembly factor 4 (SDHAF4) is downregulated in cardiac muscle in response to pathological stresses and in diseased hearts from human patients. Cardiac loss of Sdhaf4 suppresses complex II assembly and results in subunit degradation and complex II deficiency in fetal mice. These defects are exacerbated in young adults with globally impaired metabolic capacity and activation of dynamin-related protein 1, which induces excess mitochondrial fission and mitophagy, thereby causing progressive dilated cardiomyopathy and lethal heart failure in animals. Targeting mitochondria via supplementation with fumarate or inhibiting mitochondrial fission improves mitochondrial dynamics, partially restores cardiac function and prolongs the lifespan of mutant mice. Moreover, the addition of fumarate is found to dramatically improve cardiac function in myocardial infarction mice. These findings reveal a vital role for complex II assembly in the development of dilated cardiomyopathy and provide additional insights into therapeutic interventions for heart diseases.

2022-08-12 | MTBLS4579 | MetaboLights

Cardiac fibroblasts of dilated cardiomyopathy patients

Project description:Cardiac fibroblasts of dilated cardiomyopathy patients

| PRJNA926632 | ENA

Expression profile of COUP-TFII overexpressing hearts

Project description:Increased COUP-TFII levels are found in human dilated cardiomyopathy as well as in mouse models that develop cardiomyopathy. COUP-TFII overexpression in adult mouse hearts caused ventricular dilation and compromised cardiac functions. To gain insights on COUP-TFII’s effect in hearts, we identified the molecular profile of COUP-TFII overexpressing hearts through microarray analysis. The result may shred light on molecular mechanisms that mediate development of dilated cardiomyopathy.

2015-07-24 | GSE63759 | GEO

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