Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Integrated analysis of proteomics on rat hearts with aging and hypertension

ABSTRACT: Hypertension is a most important risk factor of cardiovascular diseases (CVD), and its incidence is greatest among older adults, which indicates that aging is an independent risk for both hypertension and CVD. To date, the studies on the proteomics and phosphoproteomics of the aged hypertensive hearts for studying their impacts on the pathogenesis of CVD are limited. Here we present a dataset by using proteomics and phosphor-proteomics analysis on young and aged healthy and spontaneous hypertensive (SHR) rats. The dataset has following features: 1) numerical description of average 4000 total proteins and 1500 phosphor-proteins of detectable proteins in each group; 2) proteomic and phosphoproteomic profiles of their expression patterns; 3) Pathways for individual factor (age or hypertension) and their interaction and association with CVDs. Therefore, the integrated analysis of the dataset revealed the underlying pathways of aging and/or hypertension and their interaction on cardiovascular remodelling. In summary, the dataset provides a searchable multi-omics for the researchers to explore the interaction of aging and hypertension on the pathogenesis of CVD.

INSTRUMENT(S): Q Exactive HF

ORGANISM(S): Rattus Norvegicus (rat)

TISSUE(S): Heart

SUBMITTER: Tangting Chen

LAB HEAD: Xiaoqiu Tan

PROVIDER: PXD026773 | Pride | 2021-06-18

REPOSITORIES: Pride

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	HFX3_FFRA19H100464-1A.raw	Raw
	HFX3_FFRA19H100465-1A.raw	Raw
	HFX3_FFRA19H100466-1A.raw	Raw
	HFX3_FFRA19H100467-1A.raw	Raw
	HFX3_FFRA19H100468-1A.raw	Raw

Items per page:

1 - 5 of 28

Similar Datasets

Integrated analysis of proteomics and phosphoproteomics on rat hearts with aging and hypertension

Project description:Hypertension is a most important risk factor of cardiovascular diseases (CVD), and its incidence is greatest among older adults, which indicates that aging is an independent risk for both hypertension and CVD. To date, the studies on the proteomics and phosphoproteomics of the aged hypertensive hearts for studying their impacts on the pathogenesis of CVD are limited. Here we present a dataset by using proteomics and phosphor-proteomics analysis on young and aged healthy and spontaneous hypertensive (SHR) rats. The dataset has following features: 1) numerical description of average 4000 total proteins and 1500 phosphor-proteins of detectable proteins in each group; 2) proteomic and phosphoproteomic profiles of their expression patterns; 3) Pathways for individual factor (age or hypertension) and their interaction and association with CVDs. Therefore, the integrated analysis of the dataset revealed the underlying pathways of aging and/or hypertension and their interaction on cardiovascular remodelling. In summary, the dataset provides a searchable multi-omics for the researchers to explore the interaction of aging and hypertension on the pathogenesis of CVD.

2021-06-18 | PXD026608 | Pride

Differential gene expression in the stellate ganglia of 16 week wistar and spontaneously hypertensive rat samples

Project description:Hypertension remains a poorly understood condition, and the understanding of the sympathetic nervous systems role in this disease remains even more limited. In this study, RNA-sequencing is used to identify transcriptomal differences in the sympathetic stellate ganglia between the 16-week-old normotensive wistar strain and the spontaneously hypertensive rat strain.This dataset should allow for further molecular characterisation of hypertensive changes in a cardiac-innervating sympathetic ganglion.

2018-06-21 | GSE110197 | GEO

Analysis of gene expression of LPS-stimulated monocyte from CAD patients

Project description:Data for the publication 'Identification of a Gene Network Driving the Attenuated Monocyte Response to Lipopolysaccharide of Hypertensive Coronary Artery Disease Patients'. Dissection of the impact of CVD risk factors on monocyte phenotype at the gene expression level, and in particular on their response to trauma and infection response. For any questions about the dataset, please contact Erik Biessen‘s Lab, Department of Pathology, Cardiovascular Research Institute Maastricht (CARIM), Maastricht University Medical Center, Maastricht, Netherlands

2023-06-11 | GSE234398 | GEO

Podocytes from Hypertensive and Obese Mice Acquire an Inflammatory, Senescent and Aged Phenotype

Project description:Patients with hypertension or obesity can develop glomerular dysfunction characterized by injury and depletion of podocytes. To better understand the molecular processes involved, young mice were treated with either deoxycorticosterone acetate (DOCA) or fed a high-fat diet (HFD) to induce hypertension or obesity, respectively. The transcriptional changes associated with these phenotypes were measured by unbiased bulk mRNA-sequencing of isolated podocytes from experimental models and their respective controls. Key findings were validated by immunostaining. In addition to a decrease in canonical proteins and reduced podocyte number, podocytes from both hypertensive and obese mice exhibited a sterile inflammatory phenotype characterized by increases in NLRP3 inflammasome, protein cell death-1, and Toll-Like Receptor pathways. Finally, although the mice were young, podocytes in both models exhibited increased expression of senescence and aging genes, including genes consistent with a senescence-associated secretory phenotype. However, there were differences between the hypertension- and obesity-associated senescence phenotypes. Both show stress-induced podocyte senescence characterized by increased p21 and p53. Moreover, in hypertensive mice, this is superimposed upon age-associated podocyte senescence characterized by increased p16 and p19. These results suggest that senescence, aging, and inflammation are critical aspects of the podocyte phenotype in experimental hypertension and obesity in mice.

2024-07-03 | GSE255723 | GEO

Comparative proteomic analysis in microdissected renal vessels of hypertensive and normotensive rats

Project description:Systemic hypertension has a profound impact on the renal vascular physiology. In order to elucidate the biological pathways and macromolecules deregulated by hypertension renal vessels were obtained by Laser Capture Microdissection (LCM) from Spontaneously Hypertensive Rats (SHR) and age-matched controls (20 weeks). Proteomic analysis was performed aiming to detect early molecular alterations associated with hypertension at the renal vessels before the onset of vascular damage. Proteomic analysis identified 688 proteins, of which 58 were differentially expressed (15 up-regulated and 43 down-regulated in SHR). Many of these proteins are involved in vascular tone regulation by modulating the activity of endothelial Nitric Oxide Synthase (eNOS) (e.g. Xaa-Pro aminopeptidase 1 (XPP1), N(G) N(G)-dimethylarginine dimethylaminohydrolase 1 (DDAH1), Dehydropteridine reductase (DHPR)) or in blood pressure control by regulating the renin-angiotensin system (e.g. Glutamyl aminopeptidase/Aminopeptidase A (AMPE), Aminopeptidase N (AMPN)). Moreover, pathway enrichment analysis revealed that the eNOS activation pathway is deregulated only in SHR. Our study demonstrates that hypertension causes early proteomic changes in the renal vessels of SHR. These changes are relevant to vascular tone regulation and consequently may be involved in the development of vascular damage and hypertensive nephrosclerosis. Therefore, the identified proteins could be considered as therapeutic targets.

2022-03-03 | PXD008792 | Pride

Serum metabolomics and proteomics to study the antihyperten-2 sive effect of Tenebrio molitor extracts

Project description:This study aimed at integrating metabolomics and proteomics data for a comprehensive view of the molecular targets of intervention of protein extracts from Tenebrio molitor in treating hypertension. Serum samples from spontaneously hypertensive rats and Wistar Kyoto rats were analyzed using a quantitative metabolomics and label-free proteomics approach based on liquid chromatography coupled with high resolution mass spectrometry (LC-HRMS). Among deregulated metabolites and proteins in hypertensive rats, we found 15 metabolites and 17 proteins that were restored by supplementation with Tenebrio molitor protein extract. The combination of metabolomics and proteomics provided useful data to uncover the molecular targets of intervention and the underlying functional mechanism of Tenebrio molitor protein extract in an animal model such as spontaneously hypertensive rats. The results suggested that Tenebrio molitor supplementation could effectively treat hypertension, partially by regulating proteins and molecules mainly involved in biological pathways associated to angiotensinogen-angiotensin, Serin protease inhibitors, kallikrein–kinin, reactive oxygen scavenging, and lipid peroxidation.

2022-10-13 | PXD034456 | Pride

Metabolomic Signature of Early Vascular Aging (EVA) in Hypertension

Project description:<p>Arterial stiffening is a hallmark of early vascular aging (EVA) syndrome and an independent predictor of cardiovascular morbidity and mortality. In this case-control study we sought to identify plasma metabolites associated with EVA syndrome in the setting of hypertension. An untargeted metabolomic approach was used to identify plasma metabolites in an age-, BMI- and sex-matched groups of EVA (n = 79) and non-EVA (n = 73) individuals with hypertension. After raw data processing and filtration, 497 putative compounds were characterized, out of which 4 were identified as lysophosphaditylcholines (LPCs) [LPC (18:2), LPC (16:0), LPC (18:0) and LPC (18:1)]. A main finding of this study shows that identified LPCs were independently associated with EVA status. Although LPCs have been shown previously to be positively associated with inflammation and atherosclerosis, we observed that hypertensive individuals characterized by 4 down-regulated LPCs had 3.8 times higher risk of EVA compared to those with higher LPC levels (OR = 3.8, 95% CI 1.7 – 8.5, P < .001). Our results provide new insights into a metabolomic phenotype of vascular aging and warrants further investigation of negative association of LPCs with EVA status. This study suggests that LPCs are potential candidates to be considered for further evaluation and validation as predictors of EVA in patients with hypertension </p>

2020-01-14 | MTBLS1359 | MetaboLights

Effect of Hypertension of Dendritic Cell Gene Expression

Project description:Oxidative injury and inflammation have been implicated in the genesis of hypertension but the mechanisms involved are not fully understood. We describe a new pathway in which angiotensin II promotes dendritic cell (DC) activation of T cells and ultimately hypertension. NADPH oxidase-dependent superoxide production is increased 5-fold in DCs isolated from hypertensive mice as compared to sham-treated mice. This is associated with DC accumulation of protein-isoketal adducts and production of IL-6, IL-1Î² and IL-23. DCs from hypertensive mice but not sham mice promote survival and proliferation of CD8+ T cells in culture. Chemically diverse isoketal scavengers not only prevent activation and immunogenicity of DCs, but also attenuate angiotensin II-induced hypertension. Moreover, adaptive transfer of DCs from hypertensive mice prime development of hypertension in response to a subpressor dose of angiotensin II. Exposure of DCs to tert butyl hypdroperoxide promoted isoketal formation, DC stimulation of CD8+ T cell proliferation and primed hypertension in response to low dose angiotensin II. Serum isoprostanes, precursors to isoketals, were found to be elevated in humans with treated hypertension and were markedly elevated in patients with resistant hypertension. These studies show that angiotensin II-induced hypertension activates DCs, in large part by causing superoxide production and formation of isoketals. They define a new mechanism of hypertension and identify a potential new therapeutic approach for this disease. We used microarrays to detail the expression differences in dendritic cells under hypertensive conditions. Dendritic cells were isolated from mosue spleen and subsequently treated with Angiotensin II with or without co-treatment with 2-hydroxybenzylamine (2-HOBA) for RNA extraction and hybridization on Affymetrix microarrays. We sought to determine the effect of oxidative stress on dendritic cell expression profiles.

2014-07-16 | E-GEOD-59422 | biostudies-arrayexpress

Effect of Hypertension of Dendritic Cell Gene Expression

Project description:Oxidative injury and inflammation have been implicated in the genesis of hypertension but the mechanisms involved are not fully understood. We describe a new pathway in which angiotensin II promotes dendritic cell (DC) activation of T cells and ultimately hypertension. NADPH oxidase-dependent superoxide production is increased 5-fold in DCs isolated from hypertensive mice as compared to sham-treated mice. This is associated with DC accumulation of protein-isoketal adducts and production of IL-6, IL-1β and IL-23. DCs from hypertensive mice but not sham mice promote survival and proliferation of CD8+ T cells in culture. Chemically diverse isoketal scavengers not only prevent activation and immunogenicity of DCs, but also attenuate angiotensin II-induced hypertension. Moreover, adaptive transfer of DCs from hypertensive mice prime development of hypertension in response to a subpressor dose of angiotensin II. Exposure of DCs to tert butyl hypdroperoxide promoted isoketal formation, DC stimulation of CD8+ T cell proliferation and primed hypertension in response to low dose angiotensin II. Serum isoprostanes, precursors to isoketals, were found to be elevated in humans with treated hypertension and were markedly elevated in patients with resistant hypertension. These studies show that angiotensin II-induced hypertension activates DCs, in large part by causing superoxide production and formation of isoketals. They define a new mechanism of hypertension and identify a potential new therapeutic approach for this disease. We used microarrays to detail the expression differences in dendritic cells under hypertensive conditions.

2014-07-16 | GSE59422 | GEO

Endothelial Transcriptome Remodeling in a Mouse Model of Chronic Hypertension

Project description:Aims: Hypertension poses a significant challenge to vasculature homeostasis and stands as the most common cardiovascular disease in the world. Its effects are especially profound on vasculature-lining endothelial cells that are directly exposed to the effects of excess pressure. Here, we characterize the in vivo transcriptomic response of cardiac endothelial cells to hypertension using the spontaneous hypertension mouse model BPH/2J. Methods and results: Verification of defective endothelial function in the BPH/2J hypertensive mouse strain was followed by acute isolation of cardiac endothelial cells and transcriptional profiling using RNA sequencing. Gene profiles from normotensive BPN/3J mice were compared to hypertensive animals. We observed over 3000 transcriptional differences between groups including pathways consistent with the cardiac fibrosis found in hypertensive animals. Importantly, many of the fibrosis-linked genes also differ between juvenile pre-hypertensive and adult hypertensive BPH/2J mice, suggesting that these transcriptional differences are hypertension-related. We also show that blood pressure normalization with amlodipine resulted in a subset of genes reversing their expression pattern, supporting the hypertension-dependency of altered gene expression. Yet, other transcripts were recalcitrant to therapeutic intervention illuminating the possibility that hypertension may irreversibly alter some endothelial transcriptional patterns. Conclusions: Hypertension has a profound effect on both function and transcription of endothelial cells, the latter of which was only partially restored with normalization of blood pressure. This study represents one of the first to quantify how endothelial cells are reprogrammed at the molecular level in cardiovascular pathology and advances our understanding of the transcriptional events associated with endothelial dysfunction.

2018-04-09 | GSE104530 | 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