Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Heart ventricles proteomic profile in pulmonary arterial hypertension

ABSTRACT: Arterial pulmonary hypertension is a rare disease, with little knowledge regarding its etiology, and high mortality. Development of right and later on also left ventricular heart insufficiency, secondary to pulmonary hypertension, is a negative predictive factor. Genetic and molecular processes underlying left heart ventricle remodeling over the course of pulmonary hypertension remain unknown. In particular, there is no knowledge regarding the mechanisms of left heart ventricle atrophy which was completely avoided by researchers until recently.The aim of this study was to assess changes in protein abundance in left and right heart ventricle free wall of rats in monocrotaline model of PAH.

INSTRUMENT(S): Velos Plus

ORGANISM(S): Rattus Norvegicus (rat)

TISSUE(S): Heart

DISEASE(S): Pulmonary Hypertension

SUBMITTER: Maciej Suski

LAB HEAD: Rafał Olszanecki

PROVIDER: PXD015896 | Pride | 2020-09-07

REPOSITORIES: Pride

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	15MK1L.raw	Raw
	15MK1L.tandem.pep.xml	Pepxml
	15MK1L_B.raw	Raw
	15MK1L_B.tandem.pep.xml	Pepxml
	15MK1L_B_comet.pep.xml	Pepxml

Items per page:

1 - 5 of 240

Publications

Myocardial proteomic profile in pulmonary arterial hypertension.

Hołda Mateusz K MK Stachowicz Aneta A Suski Maciej M Wojtysiak Dorota D Sowińska Natalia N Arent Zbigniew Z Palka Natalia N Podolec Piotr P Kopeć Grzegorz G

Scientific reports 20200901 1

Pulmonary arterial hypertension (PAH) is a rare, fatal, and incurable disorder. Although advances in the understanding of the PAH pathobiology have been seen in recent years, molecular processes underlying heart remodelling over the course of PAH are still insufficiently understood. Therefore, the aim of this study was to investigate myocardial proteomic profile of rats at different stages of monocrotaline-induced PAH. Samples of left and right ventricle (LV and RV) free wall collected from 32 W ...[more]

PMID: 32873862

Similar Datasets

Effect of pulmonary hypertension due to left heart disease on gene expression in pulmonary arteries

Project description:Pulmonary hypertension worsens outcome in left heart disease. Stiffening of the pulmonary artery may drive this pathology by increasing right ventricular dysfunction and lung vascular remodeling. We showed that pulmonary arteries from patients with left heart disease are characterized by increased stiffness that correlates with impaired pulmonary hemodynamics. Pulmonary arteries in left heart disease patients with pulmonary hypertension were characterized by degradation of elastic fibers paralleled by an accumulation of fibrillar collagens. We utilized RNA sequencing to identify differentially expressed genes regulating extracellular matrix remodeling in pulmonary arteries of left heart disease patients with or without pulmonary hypertension, in comparison to healthy-heart donor controls. As such we identified that transcriptional deregulation of extracellular matrix constituents and their regulators precedes clinical pulmonary hypertension, and therefore might be a pathomechanism that drives pulmonary arterial remodeling and stiffening in left heart disease.

2023-07-03 | GSE236251 | GEO

A common gene signature of the right ventricle in failing rat and human hearts

Project description:The molecular mechanisms of progressive right heart failure are incompletely understood. We systematically examined transcriptomic changes occurring over months in isolated cardiomyocytes or whole heart tissues from failing right and left ventricles in rat models of pulmonary artery (PAB) or aortic banding (AOB). Detailed bioinformatics analyses resulted in the identification of gene signatures, protein, and transcription factor networks specific to ventricles and compensated or decompensated disease states. Proteomic and RNA-FISH analyses confirmed PAB-mediated regulation of key genes (including proenkephalin) and revealed spatially heterogeneous mRNA expression in the heart. Intersection of rat PAB-specific gene sets with transcriptome data sets from human patients with chronic thromboembolic pulmonary hypertension led to the identification of more than 50 genes whose expression levels correlated with the severity of right heart disease, including multiple matrix-regulating and secreted factors. These data define a conserved, differentially regulated genetic network associated with right heart failure in rats and humans

2024-04-11 | PXD047022 | Pride

Gene expression in rat right ventricles during chronic pulmonary embolism

Project description:Pulmonary vascular occlusions due to thromboemboli can result in pulmonary hypertension and right heart damage. Treatments to clear the vascular obstructions such as i.v. heparain or thrombolytics can resolve the hypertension but right ventricular damage often occurs first. Methods of protecting the right ventricle from hypertensive damage during the course of acute treatment to clear the thromboemboli are needed. Monocyte- and neutrophil-mediated inflammation and fibrosis are associated with chronic right ventricular damage but the pathways involved are not understood. A comprehesive survey of gene expression during chronic pulmonary embolism verses control rats has been conducted in this study.

2009-09-01 | GSE11851 | GEO

Identification of right heart-enriched genes in a murine model of chronic outflow tract obstruction

Project description:The right ventricle (RV) differs in several aspects from the left ventricle (LV) including its embryonic origin, physiological role and anatomical design. In contrast to LV hypertrophy, little is known about the molecular circuits, which are activated upon RV hypertrophy (RVH). We established a highly reproducible model of RVH in mice using pulmonary artery clipping (PAC), which avoids detrimental RV pressure overload and thus allows long-term survival of operated mice. Magnetic resonance imaging revealed pathognomonic changes with striking similarities to human congenital heart disease- or pulmonary arterial hypertension- patients. Comparative, microarray based transcriptome analysis of right- and left-ventricular remodeling identified distinct transcriptional responses to pressure-induced hypertrophy of either ventricle, which were mainly characterized by stronger transcriptional responses of the RV compared to the LV myocardium. Hierarchic cluster analysis revealed a RV- and LV-specific pattern of gene activity after induction of hypertrophy, however, we did not find evidence for qualitatively distinct regulatory pathways in RV compared to LV. Data mining of nearly three thousand RV-enriched genes under PAC disclosed novel potential (co)-regulators of long-term RV remodeling and hypertrophy. We reason that specific inhibitory mechanisms in RV restrict excessive myocardial hypertrophy and thereby contribute to its vulnerability to pressure overload. Alternative splicing and gene expression analysis during development of the heart and cardiomyoyte differentiation.

2011-07-07 | E-GEOD-30428 | biostudies-arrayexpress

Expression data from lungs of rats with pulmonary hypertension

Project description:Pulmonary hypertension is a frequent consequence of left heart disease and congestive heart failure (CHF) and causes extensive lung vascular remodelling which leads to right ventricular failure. Functional genomics underlying this structural remodelling are unknown but present potential targets for novel therapeutic strategies. We used microarrays to detail the gene expression underlying vascular remodeling in the pathogenesis of pulmonary hypertension and identified distinct classes of up-regulated genes during this process. Control rat lung samples were compared to samples of aortic banding rat lungs which exhibit pulmonary hypertension

2009-06-16 | E-GEOD-16624 | biostudies-arrayexpress

Expression data from lungs of rats with pulmonary hypertension

2009-06-16 | GSE16624 | GEO

Expression data from human heart right ventricular wall

Project description:Gene expression in the right ventricle is different in control patients as compared to either idiopathic dilated cardiomyopathy or pulmonary arterial hypertension Two human hearts obtained at autopsy from each of control, pulmonary hypertension, and dilated cardiomyopathy

2015-04-02 | E-GEOD-67492 | biostudies-arrayexpress

Comparative Proteomics Reveals the Mechanism of Myocardial Adaptation to Chronic Hypoxic Injury

Project description:Congenital heart disease is a congenital defect with a very high morbidity and mortality rate, of which Cyanotic Congenital Heart Disease (CCHD) is the most severe type.Due to the special anatomical changes of CCHD, the blood of the right ventricle cannot enter the pulmonary capillaries for full oxygenation, directly flows into the left ventricle and further flows into the systemic circulation, resulting in long-term hypoxia.Therefore, the study of the injury mechanism of cardiomyocytes under chronic hypoxia may provide a new treatment strategy for patients with cyanotic coronary heart disease.Mouse cardiomyocytes(CMCs) were treated with hypoxia for different periods of time (oh, 24h, 48h and 72h, respectively), followed by label free proteomic analysis.

2024-06-22 | PXD042055 | Pride

Gene expression profile in the rat heart across hear regions [array]

Project description:To characterize a expression patterns in the heart, we used rat. 12 Wistar male rats (8 - 11 weeks) were sacrificed. Left atrium (LA) adjacent to the pulmonary vein (PV), a mass of left ventricle (LV), and free-wall of the right ventricle (RV) was isolated. Each LV mass was dissected into three pieces as samples. Because the SAN isolation procedure takes approximately 20 minutes, SA was isolated separately. The SA region was delimited by the borders of the crista terminalis, the interatrial septum, the superior vena cava, and right atrium (RA). In addition to PV, LV, RV, SA, and RA samples, pulmonary arteries were added to the samples for the rat microarray.

2022-06-22 | GSE203369 | GEO

Ventricle-specific myocardial protein and metabolite characterisation in healthy humans, with differential regulation in end-stage cardiomyopathies

Project description:The left and right ventricles of the human heart are functionally and developmentally distinct such that genetic or acquired insults can cause dysfunction in one or both ventricles resulting in heart failure. First, we performed unbiased quantitative mass spectrometry on the myocardium of 25-27 pre-mortem cryopreserved non-diseased human hearts to compare the metabolome and proteome between the normal left and right ventricles. Constituents of gluconeogenesis, glycolysis, lipogenesis, lipolysis, fatty acid catabolism, the citrate cycle and oxidative phosphorylation were down-regulated in the left ventricle, while glycogenesis, pyruvate and ketone metabolism were up-regulated. Inter-ventricular significance of these metabolic pathways was then found to be diminished within end-stage dilated cardiomyopathy and ischaemic cardiomyopathy (n = 30-33), while heart failure-associated pathways were increased in the left ventricle relative to the right within ischaemic cardiomyopathy, such as fluid sheer-stress, increased glutamine to glutamate ratio, and down-regulation of contractile proteins indicating a left ventricular pathological bias.

2024-11-06 | PXD042155 | Pride

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