Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Quancat based proteomics identifies distinct patterns of protein synthesis induced by hypertrophic agents in cardiomyocytes

ABSTRACT: The aim of this project was to quantify the effects of different hypertrophic stimuli on synthesis of specific proteins in adult rat ventricular cardiomyocytes

INSTRUMENT(S): LTQ Orbitrap Elite

ORGANISM(S): Rattus Norvegicus (rat)

TISSUE(S): Heart

SUBMITTER: Antigoni Manousopoulou

LAB HEAD: Spiros D Garbis

PROVIDER: PXD004127 | Pride | 2016-08-17

REPOSITORIES: Pride

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	12AUG14_InsRapa_1.msf	Msf
	12AUG14_InsRapa_1.pep.xml	Pepxml
	12AUG14_InsRapa_2.msf	Msf
	12AUG14_InsRapa_2.pep.xml	Pepxml
	12AUG14_InsRapa_2.raw	Raw

Items per page:

1 - 5 of 42

Similar Datasets

Neonatal rat ventricular cardiomyocytes Cells: Control vs. hypertrophic cardiomyocytes induced by isoproterenol

Project description:the expression characteristics of lncRNAs among hypertrophic cardiomyocytes induced by isoproterenol in rat ventricular myocytes from newborn Sprague-Dawley rats.

2021-04-13 | GSE169580 | GEO

Quantitative non-canonical amino acid tagging based proteomics identifies distinct patterns of protein synthesis rapidly induced by hypertrophic agents in cardiomyocytes revealing new aspects of metabolic remodeling

Project description:cardiomyocytes undergo growth and remodeling in response to specific pathological or physiological conditions. We used pSILAC to identify newly synthesized proteins induced by these stimuli.

2018-08-13 | PXD004593 | Pride

Neonatal rat ventricular cardiomyocytes Cells: Control vs. hypertrophic cardiomyocytes induced by isoproterenol

Project description:Neonatal rat ventricular cardiomyocytes Cells: Control vs. hypertrophic cardiomyocytes induced by isoproterenol

| PRJNA717037 | ENA

Adult ventricular cardiomyocytes

Project description:Adult ventricular cardiomyocytes

| PRJNA556434 | ENA

Microarray Analysis of a Familial Hypertrophic Cardiomyopathy Mouse Model Rescued by a Phospholamban Knockout

Project description:Familial hypertrophic cardiomyopathy (FHC) is a disease characterized by ventricular hypertrophy, fibrosis, and aberrant systolic and/or diastolic function. Our laboratories have previously developed 2 mouse models that affect cardiac performance. One transgenic mouse model encodes an FHC-associated mutation in α-tropomyosin (Tm180) that displays severe cardiac hypertrophy with fibrosis and impaired physiological performance. The other model was a gene knockout of phospholamban (PLB), a regulator of calcium uptake in the sarcoplasmic reticulum of cardiomyocytes; the hearts of these mice exhibit hypercontractility with no pathological abnormalities. Previous work in our laboratories show that the hearts of mice that were genetically crossed between the Tm180 and PLB KO mice rescues the hypertrophic phenotype and improves their cardiac morphology and function. We used microarrays to detail the global program of gene expression underlying cardiac remodeling and rescue of the hypertrophic cardiomyopathic phenotype and identified distinct classes of regulated genes during this process. To understand the changes in gene expression that occur over time in these animal models (Tm180, PLB KO, Tm180/PLB KO and nontransgenic control mice), we conducted microarray analyses of left ventricular tissue at 4 and 12 months of age.

2012-12-13 | E-GEOD-42892 | biostudies-arrayexpress

Ablation of SOCS3 in Cardiomyocytes Exacerbates Cardiac hypertrophy and Dysfunction by Increasing GRP78-medieated ER Stress after pressure overload

Project description:To explore the mechanisms for SOCS3 in cardiomyocytes to regulate cardiac hypertrophic remodeling after pressure overload, we therefore performed proteomic analysis to identify novel protein targets or pathways in left ventricular samples from SOCS3 knockout (SOCS3cko) mice and their WT littermates.

2021-09-08 | PXD014946 | Pride

Base editing effectively prevents the early-onset hypertrophic cardiomyopathy in Mybpc3 mutant mice

Project description:Pathogenic variants in MYBPC3 (myosin-binding protein C3) are the leading cause of genetic hypertrophic cardiomyopathy (HCM). Currently, there is no specific and effective treatment for this disease. Base editing is an emerging modality for treating monogenic diseases; however, its effect on MYBPC3 cardiomyopathy remains unexplored. Mybpc3-R946X/R946X mice developed early-onset left ventricular hypertrophy, systolic dysfunction, ventricular dilatation, and arrythmias. SpRY-ABEmax inefficiently corrected the Mybpc3-R946X mutation. In contrast, SpRY-ABE8e increased the efficiency by 3.6-fold and retained low level off-target editing. In vivo administration of SpRY-ABE8e efficiently corrected Mybpc3-R946X mutation in cardiomyocytes and prevented heart function decline, hypertrophic cardiomyopathy, and ventricular dysfunction. The therapeutic efficacy of SpRY-ABE8e-mediated gene correction surmounted AAV-mediated Mybpc3 gene replacement.Our study unveiled the immense potential of base editing to treat fatal inherited cardiomyopathies and opened a new avenue for the therapeutic managements of inherited cardiac diseases.

2024-04-04 | GSE239872 | GEO

Exosomes derived from hypertrophic cardiomyocytes induce inflammation in macrophages via miR-155 mediated MAPK pathway.

Project description:We report the application of RNA sequencing technology for high-throughput profiling of normal cardiomyocytes-derived and hypertrophic cardiomyocytes- derived exosomes. The miRNA expression profiles were determined by high throughput miRNA sequencing, and 635 differentially expressed miRNAs were found. However, compared with the control group, 7 miRNAs were significantly differentially expressed in exosomes released from Ang II-treated cardiomyocytes. A total of 4 miRNAs were upregulated while 3 were downregulated. We used qRT-PCR to characterize relative expression levels of miR-155 and miR-212-3p to validate the data obtained through miRNA sequencing. The results obtained through qRT-PCR and miRNA sequencing were essentially identical. To elucidate the potential role of miRNAs in hypertrophic cardiomyocytes, the prediction of miRNA targets was performed and 11,637 genes were obtained. To reduce the false positives rate of target gene prediction, only the predicted targets within the 3 databases described above were further analyzed. Finally, 5,477 predicted target genes were selected for further investigation. Our results support the concept that exosomal microRNAs have emerged as important inflammatory response modulators regulating the cardiac hypertrophy.

2020-09-25 | GSE158509 | GEO

The Signature of Glucocorticoid Receptor -Dependent Hypertrophic Transcriptome in Cardiomyocytes

Project description:The Signature of Glucocorticoid Receptor -Dependent Hypertrophic Transcriptome in Cardiomyocytes

| PRJNA472587 | ENA

Comparison of neonatal and adult rat ventricular cardiomyocytes

Project description: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.

2015-01-01 | E-MTAB-2832 | 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