Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Aortic Aneurysm iTRAQ HiRIEF proteomics

ABSTRACT: Conducted proteomics on samples from patients with aortic aneurysm and from non-dilated controls. Furthermore, we investigated both patients with bicuspid aortic valves (BAV) and also the more normal tricuspid aortic valves (TAV). The aim was to elucidate the molecular mechanisms behind the higher propensity of BAV patients to develop aorta dilation and consequent aortic aneurysm.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Homo Sapiens (ncbitaxon:9606)

SUBMITTER: Janne Lehti�

PROVIDER: MSV000080837 | MassIVE | Fri Mar 31 18:53:00 BST 2017

SECONDARY ACCESSION(S): PXD003702

REPOSITORIES: MassIVE

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Publications

Mesenchymal state of intimal cells may explain higher propensity to ascending aortic aneurysm in bicuspid aortic valves.

Maleki Shohreh S Kjellqvist Sanela S Paloschi Valentina V Magné Joelle J Branca Rui Miguel Mamede RM Du Lei L Hultenby Kjell K Petrini Johan J Fuxe Jonas J Lehtiö Janne J Franco-Cereceda Anders A Eriksson Per P Björck Hanna M HM

Scientific reports 20161025

Individuals with a bicuspid aortic valve (BAV) are at significantly higher risk of developing aortic complications than individuals with tricuspid aortic valves (TAV) and defective signaling during the embryonic development and/or life time exposure to abnormal hemodynamic have been proposed as underlying factors. However, an explanation for the molecular mechanisms of aortopathy in BAV has not yet been provided. We combined proteomics, RNA analyses, immunohistochemistry, and electron microscopy ...[more]

PMID: 27779199

Similar Datasets

Aortic Aneurysm iTRAQ HiRIEF proteomics

Project description:Conducted proteomics on samples from patients with aortic aneurysm and from non-dilated controls. Furthermore, we investigated both patients with bicuspid aortic valves (BAV) and also the more normal tricuspid aortic valves (TAV). The aim was to elucidate the molecular mechanisms behind the higher propensity of BAV patients to develop aorta dilation and consequent aortic aneurysm.

2016-12-23 | PXD003702 | Pride

Epigenome analysis of ascending aorta from normal, aortic dissection and bicuspid aortic valve patients

Project description:Genome wide DNA methylation profiling of ascending aorta tissue samples from normal, aortic dissection and bicuspid aortic valve patients with aortic dilation. The Illumina Infinium 450k Human DNA methylation Beadchip was used to obtain DNA methylation profiles across more than 450,000 CpGs in ascending aorta samples. Samples included 6 normal donors, 12 patients with aortic dissection and 6 patients with bicuspid aortic valve and dilated aorta.

2019-07-11 | GSE84274 | GEO

Advanced Study of Aortic Pathology (ASAP)

Project description:BACKGROUND: The vast majority of thoracic aortic aneurysms (TAAs) are observed either together with a bicuspid aortic valve (BAV), a common congenital disorder, or in idiopathic cases such as patients with a normal tricuspid aortic valve (TAV). The main objective of our study was to identify shared and unique gene expression properties underlying the aortic dilation of BAV and TAV patients. METHODS AND RESULTS: Tissue biopsies for RNA and histological analyses were obtained from aorta of non-dilated (<40mm) and dilated (>45mm) aorta of BAV and TAV patients (in total 131 patients). Additional controls were from mammary artery of the same patients (n=88) and aorta from transplant donors (n=13). Gene expression profiles generated using Affymetrix Exon arrays were analyzed from controls and from aorta intima-media and adventitia of patients (in total 345 samples). 606 genes in aortic intima-media were found to be differentially expressed with dilation. Of these, only few (<4%) were differentially expressed in both BAV and TAV patients. Gene set enrichment analysis identified cell adhesion and extracellular region gene ontology sets as common features of TAA in BAV and TAV patients. The set of immune response genes was observed to be particularly overexpressed in aortic media of dilated TAV samples. CONCLUSION: The divergent gene expression profiles indicate fundamental differences in TAA etiology of BAV and TAV patients. Immune response activation solely in the aorta media of TAV patients suggests that inflammation is a causal factor of TAA in this patient group. Biobank of patient material. Each tissue sample is from a different patient as indicated by patient ID.

2016-01-15 | E-GEOD-26155 | biostudies-arrayexpress

Development of gene expression signatures of ascending aorta of the patients with bicuspid aortic valve compared to tricuspid aortic valve.

Project description:Bicuspid aortic valve is well known as a risk factor of dilation of ascending aorta. But the mechanisms of dialation are unknown. Morever, patients with bicuspid aortic valve tend to be aortic valve disease at younger age. After aortic valve surgery, if ascending aorta is dilated, the patient must be performed re-operation. For that reason, surgery for aortic root or ascending aorta is recommended to patient with bicuspid aortic valve with dilated ascending aorta. We thought that abnormality of cell cycle of the structure protein participated in ascending aorta dilation of patient with bicuspid aortic valve. We resected the wall of the ascending aota from patient undergoing aortic valve replacement for aortic valve stenosis during operation, and performed immunohistochemical staining for akt. Anti Akt antibodys were stained much on aortic media with bicuspoed aortic valve. Akt is a protein that is involved in mTOR / PI3K, and modulate the cell differenciation and proliferation. Further, the same samples were analyzed using a microarray method. On bicuspid aortic valve patients, the expression of TSC2 is reduced, and GβL is increased. TSC2 inhibit this pathway, and MLST8 activate this pathway. In the ascending aorta of BAV patients, PI3K / mTOR system is considered to be activated. When this pathway is activated, cell proliferation and cytodifferentiation are promoted abnormally,

2017-06-30 | GSE83675 | GEO

Advanced Study of Aortic Pathology (ASAP)

2016-01-15 | GSE26155 | GEO

Gene expression changes in human thoracic and abdominal aortic aneurysm tissue

Project description:To determine how gene expression is altered in aorta tissue in response to aortic aneurysm disease. Thoracic or abdominal aorta tissue was isolated from patients requiring surgery due to aortic aneurysm or other (control) reason.

2024-10-09 | GSE202267 | GEO

Epigenome analysis of aorta from normal and Stanford-A aortic dissection patients

Project description:Genome wide DNA methylation profiling of normal and ascending aorta tissue samples from normal and aortic dissection patients. The Illumina Infinium 450k Human DNA methylation Beadchip was used to obtain DNA methylation profiles across approximately 485,512 CpGs in ascending aorta tissue samples. Samples included 4 normal donors and 4 patients with aortic dissection.

2022-11-02 | GSE202047 | GEO

The para-aortic splanchnopleure (P-Sp) of mouse embryos

Project description:The hematopoietic stem cells (HSCs) arise from hemogenic endothelial cells (HECs) in the para-aortic splanchnopleure (P-Sp)/aorta-gonad-mesonephros (AGM) region of mouse embryos. HECs differentiate into HSC precursors and blood progenitors and form intra-aortic hematopoietic clusters (IAHCs) in the aorta. To identify HECs in distinction from endothelial cells, we performed single-cell RNA-seq analysis of cells isolated from the dorsal aorta and its surrounding tissues at E9.5. We found the population of HECs in the arterial endothelial cell cluster. Therefore, our data might elucidate the mechanism of HEC development.

2024-10-16 | GSE271523 | GEO

Aorta transcriptome of ApoE-/- mice exposed to mainstream cigarette smoke for 30 days.

Project description:Aorta gene expression profiles of smoke- and sham-exposed female ApoE-/- mice were analyzed to elucidate the biological networks perturbed by exposure to 600mg TPM/m3 for 4h per day, 5 days a week, for a period of 30 days. Aortic arches were dissected 24h after the last exposure.

2015-01-12 | E-MTAB-1696 | biostudies-arrayexpress

Increased vascular smooth muscle cell senescence in aneurysmal Fibulin-4 mutant mice

Project description:Aortic aneurysms are dilations of the aorta that can rupture when left untreated. We used aneurysmal Fibulin-4R/R to further unravel the underlying mechanisms of aneurysm formation. RNA sequencing of 3-month-old Fibulin-4R/R aortas revealed significant upregulation of senescence-associated secretory phenotype (SASP) factors and key senescence factors, indicating involvement of senescence. Analysis of aorta histology and of vascular smooth muscle cells (VSMCs) in vitro confirmed the senescent phenotype of Fibulin-4R/R VSMCs by revealing increased SA-β-gal, p21 and p16 staining, increased IL-6 secretion, increased presence of DNA damage foci and increased nuclei size. Additionally, we found that p21 luminescence was increased in the dilated aorta of Fibulin-4R/R|p21-Luciferase mice. Our studies identify a cellular aging cascade in Fibulin-4 aneurysmal disease, by revealing that Fibulin-4R/R aortic VSMCs have a pronounced SASP and a senescent phenotype that may underlie aortic wall degeneration. Additionally, we demonstrated the therapeutic effect of JAK/STAT and TGF-β pathway inhibition as well as senolytic treatment on Fibulin-4R/R VSMCs in vitro. These findings can contribute to improved therapeutic options for aneurysmal disease aimed at reducing senescent cells.

2024-04-30 | GSE265869 | 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