Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Whole-transcriptome expression data from neonatal rat ventricular myocytes (NRVM) silenced for KChIP2

ABSTRACT: Loss of KChIP2 during cardiac stress has been suggested to have a transcriptional impact on cardiac ion channels contributing to maladaptive electrical remodeling. Therefore, we tested the consequence of KChIP2 loss, in the absence of cardiac stress, by treating cultured neonatal rat ventricular myocytes with shRNA for KChIP2 and subsequently performed whole-transcriptome microarray analysis to identify gene changes.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE94623 | GEO | 2017/02/20

SECONDARY ACCESSION(S): PRJNA371624

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

miRNA expression data from neonatal rat ventricular myocytes (NRVM) silenced for KChIP2

Project description:Loss of KChIP2 during cardiac stress has been suggested to have a transcriptional impact on cardiac ion channels through altered miRNA activity, contributing to maladaptive electrical remodeling. Therefore, we tested the consequence of KChIP2 loss, in the absence of cardiac stress, by treating cultured neonatal rat ventricular myocytes with siRNA for KChIP2 and subsequently performed miRNA microarray analysis to identify up-regulation of potential miRNA targets.

2017-02-20 | GSE75806 | GEO

Transcription profiling of rat neonatal ventricular myocytes

Project description:Title: Regulation of gene expression through mitogen-activated protein kinase cascades in cardiac myocytes. Description: The aim of this study is to identify the changes in gene expression induced in rat neonatal ventricular myocytes, a well-established cell culture model, by endothelin-1, a known hypertrophic agonist, and to determine which of the changes are mediated through the ERK cascade. This continues TKAC^Ys previous study of the effects of oxidative stress, which induces cardiac myocyte apoptosis.

2006-10-01 | E-MIMR-3 | biostudies-arrayexpress

Molecular Remodeling of Ion Channels in Human Atrial and Ventricular Myocytes Associated with Ischemic Cardiomyopathy

2010-02-18 | GSE17294 | GEO

Transcription profiling of phenylepherine response in rat neonatal ventricular myocytes

Project description:Title: Regulation of gene expression through mitogen-activated protein kinase cascades in cardiac myocytes. Description: We aim to identify the changes in gene expression induced in rat neonatal ventricular myocytes, a well established cell culture model, by phenylepherine, a known hypertrophic agonist, and to determine which of the changes are mediated through the ERK cascade. In addition, we intend to extend the previous studies (EXP_TKAC_0102_01 and EXP_TKAC_1103_02) on endothelin-1 induced hypertrophy and the oxidative stress induced by H2O2 by using additional concentrations and timepoints.

2006-10-01 | E-MIMR-37 | biostudies-arrayexpress

Molecular Remodeling of Ion Channels in Human Atrial and Ventricular Myocytes Associated with Ischemic Cardiomyopathy

Project description:Ischemic cardiomyopathy (ICM) leads to congestive heart failure and can cause sudden cardiac death due to arrhythmia. Existing molecular knowledge base of ICM is rudimentary because of lack of specific attribution to cell type and function. This study was designed to investigate cell-specific molecular remodeling of ion channels, exchangers and pumps, which are signaling molecules (SM) involved in electrical, signaling and mechanical functions of the heart. Atrial and ventricular myocytes were isolated by laser-capture microdissection from left atrium and ventricle of healthy and ICM human hearts. SM and their splice variants altered by ICM in cardiomyocytes were identified by splice microarray and validated by RT-PCR. Molecular profiling of ICM-related changes showed that SM in atrial and ventricular myocytes remodel following their unique programs. ICM affected 63 genes in ventricular myocytes and 12 genes in atrial myocytes. Only few of the identified genes were previously linked to human cardiac disfunctions. In our experiments we used 3 healthy hearts rejected from transplantation procedure and explanted ICM hearts from three male patients. Tissue samples were dissected from left ventricle and left atrial appendages. Atrial and ventricular myocytes were laser-capture microdissected from serial 7-8-Âµm thick cryostat sections. Individual cellular total RNA samples were analyzed on custom-built Human Ion Channel Splice Arrays slides (ExonHit) manufactured on the Ion Channel Splice Array sv1.1 platform representing 287 human SM, including 248 alternatively spliced ones in total 1655 splicing events and supplemented with capabilities to recognize connexins and ryanodine receptors.

2010-05-14 | E-GEOD-17294 | biostudies-arrayexpress

Transcription profiling by array of rat ventricular cardiac myocytes treated with interleukin 1 beta

Project description:Study of the effects of interleukin 1 beta on transcript expression in ventricular cardiac myocytes

2010-04-01 | E-MEXP-1960 | biostudies-arrayexpress

Transcription profiling of H2O2 treated rat cardiac myocytes

Project description:Title: Changes in gene expression affected by H2O2 in cardiac myocytes. Description: We aim to identify the changes in gene expression in response to oxidative stress in rat neonatal ventricular myocytes. Oxidative stress will be induced by dosing neonatal ventricular myocyte cultures with 0.2, 0.1 and 0.04mM hydrogen peroxide at 2, 4 and 8 hr time points using unstimulated myocytes as control.

2011-11-08 | E-MIMR-12 | biostudies-arrayexpress

Fibroblasts in heart scar tissue directly regulate cardiac excitability and arrhythmogenesis

Project description:Scar tissue that forms in the heart after cardiac injury, comprises an abundant number of non-excitable fibroblasts in close proximity to excitable myocytes, that are embedded within the matrix of the scar. Electrical coupling of fibroblasts and myocytes is known to occur and in vitro simulation studies have demonstrated that changes in fibroblast membrane potential can lead to myocyte excitability and susceptibility to arrhythmogenesis. However, the physiologic significance of electrical coupling between myocytes and fibroblasts in scar tissue, in the regulation of cardiac excitability and arrhythmogenesis in vivo is hotly debated and has never been demonstrated. Here, we genetically engineer a mouse that expresses the optogenetic cationic channel ChR2 exclusively in cardiac fibroblasts and not in cardiac myocytes. We subject the animal to cardiac injury and demonstrate that optical stimulation of scar tissue elicits cardiac excitability and induces arrhythmias. Connexin 43 (Cx43) is a gap junctional protein that is the most abundant connexin isoform in the heart and thought to mediate electrical coupling of fibroblasts and myocytes. Using genetic loss of function approaches, we show that Cx43 is not necessary for fibroblast-myocyte electrical coupling in vivo. CRISPR/Cas 9 mediated sequential deletion of the other highly expressed connexins also did not affect electrical coupling of fibroblasts and myocytes. Using computational modeling approaches, we show that gap junctional and non-gap junctional coupling mechanisms synergize in a functionally redundant manner to excite myocytes coupled to fibroblasts. These observations demonstrate that cardiac fibroblasts in scar tissue directly regulate cardiac excitability in vivo and can induce arrhythmogenesis. Our findings throw insight into the importance of electrical coupling of fibroblasts and myocytes in the genesis of scar associated cardiac arrhythmias.

2023-09-28 | GSE235434 | GEO

Expression data for effect of p300 knockdown and Doxorubicin treatment in cardiac myocytes

Project description:Role of p300 in regulation of stress-response genes in heart is not clear. Treatment with anti-cancer drug Doxorubicin causes cardiotoxicity through generation of oxidative stress in cardiac myocytes. Loss of p300 enhances cell death and apoptosis in response to Doxorubicin. The objective of this study was to determine if expression of genes regulated by oxidative stress is dependent of presence of p300. Further we investigated if protective effect of p300 against Doxorubicin was due to gene expression effects of p300. We used microarray to compare the transcriptomes of cardiac myocytes transfected with anti-p300 or non-silencing siRNA beforebefore and after exposure to Doxorubicin.

2015-10-01 | GSE42177 | GEO

Analysis of the transcriptome of adult cardiac myocytes stimulated with CTGF

Project description:Transgenic mice with cardiac-restricted overexpression of connective tissue growth factor (CTGF) have substantially increased tolerance towards ischemia/reperfusion injury. In the transgenic mouse model, we found that CTGF induces expression of severeal genes putatively involved in cardioprotection. The purpose of this study was to determine gene expression in cardiac myocytes stimulated with purified, recombinant CTGF, comparing unstimulated and stimulated samples. The cytoprotective actions of CTGF was recflected in the transcriptome of CTGF-stimulated cardiac myocytes. Gene ontology analysis revealed that genes included under the terms anti-apoptosis, response to wounding, and response to stress were significantly overrepresented in cardiac myocytes exposed to CTGF. Serveral of the most higly up-regulated genes have previously been reported to exert cardioprotective actions and increase tolerance towards ischemia/reperfusion injury. Primary, adult cardiac myocytes were cultured in the absence (n=6) or presence (n=6) of 200 nmol/L recombinant CTGF for 48 hours.

2015-02-01 | E-GEOD-36073 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data