Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Differential proteomics - Pulmonary pressure reduction attenuates expression of proteins identified by lung proteomic profiling in pulmonary hypertensive rats

ABSTRACT: Pulmonary pressure reduction attenuates expression of proteins identified by lung proteomic profiling in pulmonary hypertensive rats

INSTRUMENT(S): instrument model

ORGANISM(S): Rattus Norvegicus (rat)

SUBMITTER: Bent Honoré

PROVIDER: PRD000524 | Pride | 2011-09-28

REPOSITORIES: Pride

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	PRIDE_Exp_Complete_Ac_18476.pride.mgf.gz	Mgf
	PRIDE_Exp_Complete_Ac_18476.pride.mztab.gz	Mztab
	PRIDE_Exp_Complete_Ac_18476.xml.gz	Xml

Items per page:

1 - 3 of 3

Publications

Pulmonary pressure reduction attenuates expression of proteins identified by lung proteomic profiling in pulmonary hypertensive rats.

Østergaard Louise L Honoré Bent B Thorsen Lise B LB Baandrup Jonas J Eskildsen-Helmond Yvonne Y Laursen Britt E BE Vorum Henrik H Mulvany Michael J MJ Simonsen Ulf U

Proteomics 20111028 23

The present study was designed to analyze protein expression in lungs from pulmonary hypertensive rats in order to identify novel signaling pathways. This was achieved by proteomic studies in which proteins from lung homogenates from hypoxic were compared to normoxic rats. The expression of these proteins was then investigated in lungs from hypoxic rats treated with either an activator of soluble guanylyl cyclase, BAY 412272, or an inhibitor of phosphodiesterase type 5, sildenafil. The proteomic ...[more]

PMID: 21905223

Similar Datasets

Intermittent short-duration reoxygenation protects against simulated high altitude-induced pulmonary hypertension in rats

Project description:High-altitude pulmonary hypertension (HAPH) is a severe and progressive disease caused by chronic hypoxia and subsequent pulmonary vascular remodeling. No cure is currently available owing to an incomplete understanding about vascular remodeling. It is believed that hypoxia-induced diseases can be prevented by treating hypoxia. Thus, this study aimed to determine whether daily short-duration reoxygenation at sea level attenuates pulmonary hypertension under high-altitude hypoxia. To this end, a simulated 5,000-m hypoxia rat model was used to evaluate the effect of short-duration reoxygenation. Results show that intermittent, not continuous, short-duration reoxygenation effectively attenuates hypoxia-induced pulmonary hypertension. The mechanisms underlining the protective effects involved that intermittent, short-duration reoxygenation prevented functional and structural remodeling of pulmonary arteries and proliferation, migration, and phenotypic conversion of pulmonary artery smooth muscle cells under hypoxia. The specific genes or potential molecular pathways responsible for mediating the protective effects were also characterised by RNA sequencing.This study is novel in revealing a new potential method in preventing high-altitude pulmonary hypertension. It gives insights into the selection and optimisation of oxygen supply schemes in high-altitude areas.

2020-11-06 | GSE160926 | GEO

Hypertensive Study

Project description:Hypertensive Study

| PRJNA101737 | ENA

Integrated proteomics and metabolomics reveal the mechanisms of blood pressure reduction in spontaneously hypertensive rats under high altitude hypoxic conditions

Project description:In this study, we employed an integrated proteomic and metabolomic approach to systematically analyze the proteome and metabolome profiles of SHRs following prolonged exposure to a high-altitude hypoxic environment. Bioinformatics and enrichment analysis revealed that proteins with significant differential expression were predominantly involved in pathways such as oxidative phosphorylation, thermogenesis, TCA cycle, and carbon metabolism. Further analysis indicated that alterations in key metabolites, including thiamine, S-adenosylhomocysteine, pantothenic acid, fumaric acid, and homoserine, interact with differentially expressed proteins, collectively contributing to the modulation of blood pressure regulation in SHRs under hypoxic conditions. This research provides new molecular insights into understanding the impact of high-altitude hypoxia on the blood pressure regulatory mechanisms in spontaneously hypertensive rats.

2024-08-27 | PXD055443 |

Excessive leukotriene B4 in nucleus tractus solitarii is pro-hypertensive in spontaneously hypertensive rats.

2013-03-01 | GSE8796 | GEO

Excessive leukotriene B4 in nucleus tractus solitarii is pro-hypertensive in spontaneously hypertensive rats.

Project description:We have used Affymetrix microarray-driven gene profiling to comprehensively describe the expression of mRNAs in the nucleus tractus solitarii (NTS) in the adult male spontaneously hypertensive rat (SHR) as compared to its normotensive parental Wistar-Kyoto (WKY) strain. Keywords: Gene expression NTS was dissected from hypertensive (SHR) and normotensive (WKY) strains of rat. For each structure, 10 independent Affymetrix Genechip 230 2.0 experiments were performed (5 SHR, 5 WKY), with each chip representing an independent biological replication (n=5).

2013-03-01 | E-GEOD-8796 | biostudies-arrayexpress

A Lactobacilli-Based Inhaled Live Biotherapeutic Product Attenuates Pulmonary Neutrophilic Inflammation

Project description:A Lactobacilli-Based Inhaled Live Biotherapeutic Product Attenuates Pulmonary Neutrophilic Inflammation

| PRJNA1132278 | ENA

Altered neurotrophin expression profiles in the nucleus of the solitary tract of spontaneously hypertensive rats

Project description:Our previous findings suggest that the nucleus of the solitary tract (NTS), a pivotal region for regulating the set-point of arterial pressure, exhibits abnormal inflammation in pre-hypertensive and spontaneously hypertensive rats (SHRs) together with elevated anti-apoptotic and low apoptotic factor levels compared with that of normotensive Wistar–Kyoto (WKY) rats. Whether this chronic condition affects neuronal growth and plasticity in the NTS remains unknown. To unveil the characteristics of the neurodevelopmental environment in the NTS of hypertensive rats, we investigated the gene expression profile of neurotrophins and their receptors in SHRs compared to that of normotensive rat WKY.

2015-04-15 | GSE67874 | GEO

DNA methylation inhibition attenuates pressure overload-induced cardiac hypertrophy in rats

Project description:DNA methylation inhibition attenuates pressure overload-induced cardiac hypertrophy in rats

| PRJNA437252 | ENA

Gallic Acid Reduces Blood Pressure and Attenuates Oxidative Stress and Cardiac Hypertrophy in Spontaneously Hypertensive Rats.

Project description:Gallic acid (GA) has been reported to have beneficial effects on cancer, vascular calcification, and diabetes-induced myocardial dysfunction. We hypothesized that GA controls hypertension via oxidative stress response regulation in an animal model for essential hypertension. Spontaneously hypertensive rats (SHRs) were administered GA for 16 weeks. GA treatment lowered elevated systolic blood pressure in SHRs through the inhibition of vascular contractility and components of the renin-angiotensin II system. In addition, GA administration reduced aortic wall thickness and body weight in SHRs. In SHRs, GA attenuated left ventricular hypertrophy and reduced the expression of cardiac-specific transcription factors. NADPH oxidase 2 (Nox2) and GATA4 mRNA expression was induced in SHR hearts and angiotensin II-treated H9c2 cells; this expression was downregulated by GA treatment. Nox2 promoter activity was increased by the synergistic action of GATA4 and Nkx2-5. GA seems to regulate oxidative stress by inhibiting the DNA binding activity of GATA4 in the rat Nox2 promoter. GA reduced the GATA4-induced Nox activity in SHRs and angiotensin II-treated H9c2 cells. GA administration reduced the elevation of malondialdehyde levels in heart tissue obtained from SHRs. These findings suggest that GA is a potential therapeutic agent for treating cardiac hypertrophy and oxidative stress in SHRs.

| S-EPMC5688141 | biostudies-literature

Effect of AT1 receptor anatagonist on brain microvessels from hypertensive and normotensive rats

Project description:In hypertension, abnormal regulation of microcirculation and endothelial dysfunction enhances vulnerability to hypertensive brain damage. In addition to lowering blood pressure, blockade of Angiotensin II AT1 receptors protects against stroke and stress in different animal models and this treatment may be of therapeutic advantage. We studied gene expression using Affymetrix Rat Genome U34A arrays from brain microvessels of spontaneously hypertensive rats (SHR) and their normotensive Wistar Kyoto controls (WKY) rats treated with an AT1 antagonist (candesartan, 0.3 mg/kg/day) or vehicle via osmotic minipumps for 4 weeks. Keywords: other

2006-06-03 | GSE2739 | GEO

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