Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Comparison of neonatal and adult rat ventricular cardiomyocytes

ABSTRACT: We addressed the question of which protein kinases are expressed in cardiomyocytes. We assessed the changes during postnatal development, comparing profiles in rat neonatal ventricular cardiomyocytes (NVMs) with adult ventricular cardiomyocytes (AVMs). Neonatal and adult rat ventricular cardiomyocytes prepared according to established procedures (Marshall et al. PLoS ONE 2010 5(4):e10027; Fuller and Sugden, FEBs Lett. 1989 247:209-12; Rodrigues and Severson In Biochemical Techniques in the Heart (McNeill, J. H., Ed.) pp 101-115, CRC Press, New York.). mRNA expression profiles compared using Affymetrix rat genome 230 2.0 arrays.

ORGANISM(S): Rattus norvegicus

SUBMITTER: Angela Clerk

PROVIDER: E-MTAB-2832 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Publications

Cardiac protein kinases: the cardiomyocyte kinome and differential kinase expression in human failing hearts.

Fuller Stephen J SJ Osborne Sally A SA Leonard Sam J SJ Hardyman Michelle A MA Vaniotis George G Allen Bruce G BG Sugden Peter H PH Clerk Angela A

Cardiovascular research 20150810 1

<h4>Aims</h4>Protein kinases are potential therapeutic targets for heart failure, but most studies of cardiac protein kinases derive from other systems, an approach that fails to account for specific kinases expressed in the heart and the contractile cardiomyocytes. We aimed to define the cardiomyocyte kinome (i.e. the protein kinases expressed in cardiomyocytes) and identify kinases with altered expression in human failing hearts.<h4>Methods and results</h4>Expression profiling (Affymetrix micr ...[more]

PMID: 26260799

Similar Datasets

Regulation of total and polysomal RNA expression in rat neonatal cardiac myocytes by H2O2

Project description:We are determining the effects of oxidative stress on mRNA expression in cardiac myocytes to identify immediate early genes and establish if there is an effect of different concentrations on recruitment to polysomes for translation. Rat neonatal cardiac myocytes in primary culture were exposed to 0.2 mM H2O2 for 1 h and total or polysomal RNA prepared for microarray analysis. These samples were prepared simultaneously with others for controls, endothelin-1 and insulin that have been published (PMID: 18275597; PMID: 20509958) and these data are already publicly available (E-MIMR-681 for ET-1 data; E-MEXP-2527 for insulin data).

2018-05-17 | E-MTAB-6758 | biostudies-arrayexpress

Methylation profiling of NimbleGen Mouse DNA Methylation 3x720K CpG Island Plus RefSeq Promoter Array

Project description:NimbleGen Mouse DNA Methylation 3x720K CpG Islands Pus RefSeq Promoter Array was used to perform a DNA methylome analysis to unravel the molecular mechanism underlying the dedifferentiation and cell cycle reentry of mouse adult cardiomyocytes (ACMs). A total of six DNA samples (10 ng each) derived from the population cells from either control adult cardiomyocytes or mCPCs were subject to whole genome amplification and then 2.5 Âµg of amplified products were used for DNA methylome analysis. There were three biological replicates in each group (both ACM controls and mCPCs). The whole genome methylome data using NimbleGen Mouse 2.1M array and genomic DNA derived from population cells for both control adult cardiomyocytes and mCPC can be found in E-MTAB-3984. Single-cell whole-transcriptome microarray data using Affymetrix Mouse Genome 430 2.0 Array can be found in E-MTAB-3981.

2016-03-22 | E-MTAB-3982 | biostudies-arrayexpress

Methylation profiling of NimbleGen Mouse 2.1M Array

Project description:NimbleGen Mouse DNA Methylation 2.1M Array (CHARM design) was used to perform a DNA methylome analysis to unravel the molecular mechanism underlying the dedifferentiation and cell cycle reentry of mouse adult cardiomyocytes (ACMs). A total of six DNA samples (10 ng each) derived from population cells were subjected to whole genome amplification using Sigma WGA kit, and then 2.5 Âµg amplified DNA product was used for DNA methylome analysis. Three biological replicates of population ACM cells were used as controls and three biological replicates of population myocyte-derived progenitor cells (mCPCs) were used in the experimental group. Methylome microarray data using NimbleGen Mouse DNA Methylation 3x720K CpG Islands Pus RefSeq Promoter Array and DNA derived from population cells for both control cardiomyocytes and mCPCs can be found in E-MTAB-3982. Single-cell whole-transcriptome data using Affymetrix Mouse Genome 430 2.0 Array can be found in E-MTAB-3981.

2016-03-22 | E-MTAB-3984 | biostudies-arrayexpress

Transcription profiling by array and functional characterization of developing cardiomyocytes from recombinant murine embryonic stem cells

Project description:Here, we characterize the transcriptome of the mouse embryonic stem cell line CM7-1 during differentiation into beating cardiomyocytes and compared the gene expression profiles with those from primary adult murine cardiomyocytes and left ventricular myocardium.

2009-03-21 | E-MEXP-1405 | biostudies-arrayexpress

Transcription profiling of Affymetrix Mouse Genome 430 2.0 Array

Project description:Affymetrix Mouse Genome 430 2.0 Array was used to perform single-cell transcriptome analysis to unravel the molecular mechanisms underlying the dedifferentiation and cell cycle reentry of mouse adult cardiomyocytes (ACMs). A total of six samples were used for single-cell transcriptome analysis using Affymetrix MG 430 2.0 Array coupled with a microfluidic chip for single cell isolation and NuGen Ovation Single-Cell Amplification technologies. Three biological replicates of adult cardiomyocyte single cells were used as controls and three biological replicates of myocyte-derived progenitor single cells (mCPCs) were used in the experimental group. The whole genome methylome microarray data using NimbleGen Mouse DNA Methylation 3x720K CpG Island Plus RefSeq Promoter Array and genomic DNA derived from population cells for both control adult cardiomyocytes and mCPCs can be found in E-MTAB-3982. The whole genome methylome data using NimbleGen Mouse 2.1M array and genomic DNA derived from population cells for both control adult cardiomyocytes and mCPC can be found in E-MTAB-3984.

2016-03-22 | E-MTAB-3981 | 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

Highly efficient derivation of ventricular cardiomyocytes from induced pluripotent stem cells with a distinct epigenetic signature

Project description:The generation of sufficient numbers of mature ventricular myocytes for effective cell-based therapy is a central barrier for cardiac regenerative medicine. Here we demonstrate that induced pluripotent stem cells (iPSCs) can be derived from murine ventricular myocytes, and consistent with other reports of iPSCs derived from various somatic cell types, ventricular myocyte derived iPSCs (ViPSCs) exhibit a markedly higher propensity to differentiate into beating cardiomyocytes as compared to genetically-matched embryonic stem cells (ESCs) or iPSCs derived from tail-tip fibroblasts. Strikingly, ViPSC-derived cardiomyocytes form up to 99% ventricular myocytes suggesting that ventricular myocyte-derived iPSCs may be a viable strategy to generate specific cardiomyocyte subtypes for cell-based therapies. The enhanced ventricular myogenesis in ViPSCs is mediated via increased numbers of cardiovascular progenitors at early stages of differentiation. In order to investigate the mechanism of enhanced ventricular myogenesis from ViPSCs, we performed global gene expression and DNA methylation analysis, which revealed a distinct epigenetic signature that may be involved in specifying the ventricular myocyte fate in pluripotent stem cells. Total RNA was extracted from mouse ES cells, tail tip fibroblasts (TTFs), ventricular myocytes (VMs), TTF-derived induced pluripotent stem cells (TiPSCs) and VM-derived induced pluripotent stem cells (ViPSCs). Global gene expression profiling was performed using affymetrix mouse 430 2.0 gene arrays.

2011-10-04 | E-GEOD-32598 | biostudies-arrayexpress

Constitutive Protein Kinase G Activation Exacerbates Stress-induced Cardiomyopathy

Project description:: Heart failure is associated with high morbidity and mortality, and new therapeutic targets are needed. Preclinical data suggest that pharmacological activation of protein kinase G (PKG) can reduce maladaptive ventricular remodeling and cardiac dysfunction in the stressed heart. However, clinical trial results have been mixed, and the effects of long-term PKG activation in the heart are unknown.

2023-07-20 | PXD022600 | Pride

neonatal rat cardiomyocytes stimulated by Oncostatin M

Project description:Molecular analysis of transcriptional changes in cardiomyocytes induced by Oncostatin M treatment. The rationale of this experiment is described in [Kubin, T., et al. Oncostatin M is a major mediator of cardiomyocyte dedifferentiation and remodeling. Cell stem cell 9, 420-432 (2011)]

2015-02-27 | E-MTAB-2560 | biostudies-arrayexpress

LncRNA Chaer contributes to the transcriptome reprogramming during phenylephrine-induced hypertrophy in neonatal rat ventricular myocytes

Project description:We compared the transcriptome modified by siRNA-mediated cardiac hypertrophy associated epigenentic regulator (Chaer) with negative control siRNA treated neonatal rat ventricular myocytes with or without phenylephrine treatment. The results suggest that Chaer knockdown broadly blocks the phenylephrine-induced hypertrophic programming of the transcriptome. Transcripts profiles from neonatal rat ventricular myocytes with or without phenylephrine and with or without Chaer-specific siRNA compared to negative control siRNA

2016-06-30 | E-GEOD-82339 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

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