Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Expression data in Abdominal Aortic Aneurysms

ABSTRACT: Current clinical practice for the assessment of abdominal aortic aneurysms (AAA) is based on vessel diameter and does not account for the multifactorial, heterogeneous remodeling that results in the regional weakening of the aortic wall leading to aortic growth and rupture. This study was conducted to determine correlation between a novel non-invasive surrogate measure of regional aortic weakening and the results from invasive analyses performed on corresponding ex vivo aortic samples. Tissue samples were evaluated to classify local wall weakening and likelihood of further degeneration based on non-invasive indices. A combined, image-based fluid dynamic and in-vivo strain analysis approach was used to estimate the Regional Aortic Weakness (RAW) index and assess individual aortas of AAA patients prior to elective surgery. Nine patients were treated with complete aortic resection allowing the systematic collection of tissue samples that were used to determine regional aortic mechanics, microstructure and gene expression by means of mechanical testing, microscopy and transcriptomic analyses. The RAW index was significantly higher for samples exhibiting lower mechanical strength (p = 0.035) and samples classified with low elastin content (p = 0.020). Samples with higher RAW index had the greatest number of genes differentially expressed compared to any constitutive metric. High RAW samples showed a decrease in gene expression for elastin and a down-regulation of pathways responsible for cell movement, reorganization of cytoskeleton, and angiogenesis. Please note that the sample 'characteristisc: strain' represents the in-vivo strain corresponding to each section of aorta, which is measured from dynamic CT images of patient AAA using a proprietary software.

ORGANISM(S): Homo sapiens

PROVIDER: GSE165470 | GEO | 2021/01/26

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Gene expression profiles in Elastin (Eln+/-) mouse aorta and aortic valve tissue

Project description:Elastin wild type Eln+/+ and Eln+/- mouse aorta and aortic valve tissue. In the study, we demonstrated differential gene expression in juvenile elastin deficient mouse valve tissue. In the study, we hybridized RNA from Elastin wild type (Eln+/+) aorta tissue, elastin wild type (Eln+/+) aortic valve tissue, elastin (Eln+/-) aorta tissue and elastin (Eln+/-) aortic valve tissue to Affymetrix GeneChip Mouse Genome 430 2.0 Array

2009-11-30 | E-GEOD-16012 | biostudies-arrayexpress

Cycloastragenol inhibit experimental abdominal aortic aneurysm progression

Project description:Abstract: The pathogenesis of AAA involves vascular inflammation and oxidative stress. Astragali Radix contains cycloastragenol (CAG) known to have anti-inflammatory and anti-oxidative properties. We hypothesized that CAG supplement impairs AAA progression. AAA was induced in male rats by intraluminal elastase infusion in the infrarenal aorta and treated daily with CAG (125 mg/kg/day). Aortic expansion was followed weekly by ultrasound, with euthanization at day 28. Changes in AAA wall composition were analyzed at mRNA levels, histology, zymography and explorative proteomic analyses. At day 28, mean AAA diameter was 37% lower in CAG group (p<0.0001). In aneurysm cross sections, elastin content was insignificantly higher in CAG group (10.5% ± 5.9% vs 19.9% ± 16.8%, p=0.20) with more preserved elastin lamellae structures (p=0.0003) and with no microcalcifications. Aneurysmal matrix metalloprotease-2 activity was reduced by CAG treatment (p=0.022), and mRNA levels of inflammatory- and antioxidative markers showed no difference between groups. Explorative proteomic analysis showed no difference in protein levels when adjustment for multiple testing. Amongst unadjusted affected proteins were fibulin-5 (p=0.02), aquaporin-1 (p=0.02) and prostacyclin synthase (p=0.006). CAG impairs experimental AAA progression by reduction of elastin degradation through decreased MMP-2 activity, thus CAG could be considered tested in AAA patients.

2022-05-20 | PXD030441 | Pride

Differential gene expression in human abdominal aortic aneurysm and atherosclerosis

Project description:The aim of this study was to assess the relative gene expression in human AAA and AOD. Genome-wide expression analysis of abdominal aortic aneurysm (AAA) and aortic occlusive disease (AOD) specimens obtained from 20 patients with small AAA (mean maximum aortic diameter=54.3±2.3 mm), 29 patients with large AAA (mean maximum aortic diameter=68.4±14.3 mm), and 9 AOD patients (mean maximum aortic diameter=19.6±2.6 mm). Relative aortic gene expression was compared with that of 10 control aortic specimen of organ donors.

2015-06-30 | E-GEOD-57691 | biostudies-arrayexpress

Nicotine administration augments abdominal aortic aneurysm progression in rats

Project description:Inflammation and elastin degradation are key hallmarks in the pathogenesis of abdominal aortic aneurysms (AAA). It has been acknowledged that activation of alpha7 nicotinic acetylcholine receptors (α7nAChRs) attenuates inflammation, termed the cholinergic anti-inflammatory pathway (CAP). Thus, we hypothesized that low-dose nicotine, an α7nAChR agonist, impairs the progression of AAAs in rats by activating the CAP. Male Sprague-Dawley rats underwent surgical AAA induction with intraluminal elastase infusion. We compared vehicle rats with rats treated with nicotine (1.25 mg/kg/day) and the aneurysm progression was monitored by weekly ultrasound images for 28 days. Nicotine significantly promoted AAA progression after 28 days of treatment (p=0.031). Additionally, gelatin zymography demonstrated that nicotine significantly reduced pro-matrix metalloprotease (pro-MMP) 2(p=0.029) and MMP9(p=0.030) activity in aneurysmal tissue. No significant difference was found in elastin content or the score of elastin degradation between the groups. Neither infiltrating neutrophils nor macrophages, nor aneurysmal messenger RNA (mRNA) levels of pro- or anti-inflammatory cytokines differed between the vehicle and nicotine group. Finally, no difference in mRNA levels of markers for antioxidative stress or vascular smooth muscle cells contractile phenotype was observed. However, proteomics analyses of non-aneurysmal abdominal aortas revealed that nicotine decreased proteins in the ontology terms inflammation and reactive oxygen species and in contradiction to augmented AAAs. In conclusion, treatment with the given nicotine dose augmented AAA progression in this rat model.

2023-07-20 | PXD040414 | Pride

Association of NOTCH3 with Elastic Fiber Dispersion in the Infrarenal Abdominal Aorta of Cynomolgus Monkeys

Project description:OBJECTIVE: The regional heterogeneity of vascular components and transcriptomes is an important determinant of aortic biology. This notion has been explored in multiple mouse studies. In the present study, we examined the regional heterogeneity of aortas in non-human primates. APPROACH AND RESULTS: Aortic samples were harvested from the ascending, descending, suprarenal, and infrarenal regions of young control monkeys and adult monkeys provided with high fructose for 3 years. The regional heterogeneity of aortic structure and transcriptomes was examined by histological and bulk RNA sequencing analyses. Immunostaining of CD31 and αSMA revealed that endothelial and smooth muscle cells were distributed homogeneously across the aortic regions. In contrast, elastic fibers were less abundant and dispersed in the infrarenal aorta compared to other regions and associated with collagen deposition. Bulk RNA sequencing identified a distinct transcriptome related to the Notch signaling pathway in the infrarenal aorta with significantly increased NOTCH3 mRNA compared to other regions. Immunostaining revealed that NOTCH3 protein was increased in the media of the infrarenal aorta. The abundance of medial NOTCH3 was positively correlated with the dispersion of elastic fibers. Adult cynomolgus monkeys provided with high fructose displayed vascular wall remodeling, such as smooth muscle cell loss and elastic fiber disruption, predominantly in the infrarenal region. The correlation between NOTCH3 and elastic fiber dispersion was enhanced in these monkeys. CONCLUSION: Aortas of young cynomolgus monkeys display regional heterogeneity of their transcriptome and the structure of elastin and collagens. Elastic fibers in the infrarenal aorta are dispersed along with upregulation of medial NOTCH3.

2023-03-22 | GSE227434 | GEO

Gene expression profiles in Elastin (Eln+/-) mouse aorta and aortic valve tissue

2009-11-30 | GSE16012 | GEO

Geisinger eMERGE - Abdominal Aortic Aneurysm Project (AAAP)

Project description:<p>A large research cohort of Geisinger Abdominal Aortic Aneurysm (AAA) patients was created by enrolling and consenting patients of the Geisinger Department of Vascular Surgery. Consented patients provide blood, serum and DNA samples for research and authorize use of data in their medical record for research. They also complete a data questionnaire that asks information about family history of AAA and other vascular diseases, as well as information on known or suspected AAA risk factors, including smoking history, body mass index, hypertension, type 2 diabetes, and atherosclerotic disease. The AAA cases are 78% male, with a mean age of 74 years; 39% have undergone surgical or endovascular repair; more than 85% or current or past smokers; approximately 20% of cases report a positive family history of AAA. Geisinger AAA patients undergo regular imaging studies, typically every 6 months, to monitor the progression of aneurysm expansion. This allows the growth rates of their aneurysm to be calculated. DNA samples from a total of 910 AAA patients were used for whole genome genotyping; these results are included in the dbGaP.</p>

| phs000387 | dbGaP

Angiotensin II induced aneurysms in male ApoE mice

Project description:In this study we used microarrays to examine relative genes expression within the aorta of ApoE-/- infused with angiotensin II in relation to aneurysm formation. Infusion of angiotensin II induces aortic dilatation particularly of the suprarenal aorta in ApoE-/- mice. Based on studies carried out in our and other laboratories the response to angiotensin II is variable, with some mice developing large aneurysms but other animals appearing resistant to aneurysm formation with aortic diameters similar to that of saline controls. We compared RNA expression from whole aortas of 17 week old male ApoE-/- mice exposed to angiotensin II (1.44 Âµg/kg/min) for 4 weeks where there was clear evidence of aortic aneurysm formation (n=5) with that of mice failing to develop aneurysms (n=7) and those exposed to saline infusion (n=6). AAA was defined as diameter of suprarenal aorta greated than 1.5mm measured on photographs of aortas at necroscopy. Keywords: Disease state analysis 18 samples analysed, AAA (n=5), no AAA (n=7), saline (n=6). AAA - abdominal aortic aneurysm

2010-06-24 | E-GEOD-12591 | biostudies-arrayexpress

Sex chromosome complement defines diffuse versus focal angiotensin II-induced aortic pathology

Project description:Objective-Aortic pathologies exhibit sexual dimorphism, with aneurysms in the ascending, thoracic and abdominal aorta (AAA) exhibiting higher prevalence in males. Despite lower incidence of aortic vascular disease in women, aneurysms progress rapidly. Mechanisms for these sex differences are unclear. We defined the role of sex chromosome complement and testosterone in regional development and progression of angiotensin II (AngII)-induced vascular pathologies. Approach and Results-We used transgenic male mice expressing Sry on an autosome to create low density lipoprotein receptor (Ldlr) deficient male mice with an XY or XX sex chromosome complement. Subjects were then sham operated or orcheictomized. Transcriptional profiling on abdominal aortas from XY or XX males demonstrated1746 genes influenced by sex chromosomes, sex hormones, or an interaction. A second cohort of animals was then infused with AngII for 28 days. Diffuse aortic aneurysm pathology developed in XY AngII-infused males, while XX males developed discrete AAAs. Castration reduced all AngII-induced aortic pathologies in XY and XX males. Thoracic aortas from AngII-infused XY males, but not XX males exhibited adventitial thickening. We infused male XY and XX mice with saline or AngII and quantified mRNA abundance of key genes in thoracic versus abdominal aortas. Regional differences in mRNA abundance existed before AngII infusions, which were differentially influenced by AngII between genotypes. Prolonged AngII infusions resulted in AAA aortic wall thickening in XY males with diffuse aortic pathology, while XX males had dilated focal AAAs. Conclusions-An XY sex chromosome complement mediates diffuse aortic pathology, while an XX sex chromosome complement contributes to discrete AngII-induced AAAs.

2018-07-22 | GSE102143 | GEO

Murine Abdominal Aortic Aneurysm, PPE Model - In Vivo Modulation of miRNA-24 (Day 7)

Project description:Transcriptional profiling of infrarenal aortic tissue from Male 10-week-old C57BL/6J mice after AAA-induction with porcine pancreatic elastase, compared with sham-operated saline-injected mice. One day after AAA-induction, the mice were injected intraperitoneally with either lentiviral packaged miR-24 antagomir (anti-miR-24) or miR-24 mimic (pre-miR-24), or a scrambled microRNA control (scr-miR). Aortic samples were obtained 7 days after operation. The goal was to examine gene expression in developing AAA in this model, and to compare the effects of scr-miR, anti-miR-24 and pre-miR-24.

2014-08-31 | GSE51228 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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