Circulating microRNAs: a novel potential biomarker for diagnosing acute aortic dissection
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE92427 | GEO | 2017/11/15
SECONDARY ACCESSION(S): PRJNA357550
REPOSITORIES: GEO
Similar Datasets
Project description:Aneurysmatic and dissection cells show a specific alteration of gene expression, which allow a disease specific distinction. We used microarrays to analyse the cellular gene expression of controls, thoracic aortic aneurysm, and aortic dissection.
2022-12-02 | GSE219204 | GEO
Project description:The mechanism by which aging induces aortic aneurysm and dissection (AAD) remains unclear. A total of 430 subjects were recruited for screening of differentially expressed plasma microRNAs. We found that miR-1204 was significantly increased in both plasma and aorta of elder patients with AAD, and was positively correlated with age. Cell senescence induced the expression of miR-1204 through p53 interaction with plasmacytoma variant translocation 1, and miR-1204 induced vascular smooth muscle cell (VSMC) senescence to form a positive feedback loop. miR-1204 aggravated angiotensin II-induced AAD formation, and inhibition of miR-1204 attenuated β-aminopropionitrile monofumarate-induced AAD formation. Mechanistically, miR-1204 directly targeted myosin light chain kinase (MYLK) to promote VSMCs to acquire senescence-associated secretory phenotype (SASP) and lose their contractile phenotype. Overexpression of MYLK reversed miR-1204-induced VSMC senescence, SASP and contractile phenotype changes, and the decrease of transforming growth factor-β signaling pathway. Our findings suggest aging aggravates AAD via miR-1204-MYLK signaling axis.
2024-04-01 | PXD048658 | Pride
Project description:The mechanism by which aging induces aortic aneurysm and dissection (AAD) remains unclear. A total of 430 subjects were recruited for screening of differentially expressed plasma microRNAs. We found that miR-1204 was significantly increased in both plasma and aorta of elder patients with AAD, and was positively correlated with age. Cell senescence induced the expression of miR-1204 through p53 interaction with plasmacytoma variant translocation 1, and miR-1204 induced vascular smooth muscle cell (VSMC) senescence to form a positive feedback loop. miR-1204 aggravated angiotensin II-induced AAD formation, and inhibition of miR-1204 attenuated β-aminopropionitrile monofumarate-induced AAD formation. Mechanistically, miR-1204 directly targeted myosin light chain kinase (MYLK) to promote VSMCs to acquire senescence-associated secretory phenotype (SASP) and lose their contractile phenotype. Overexpression of MYLK reversed miR-1204-induced VSMC senescence, SASP and contractile phenotype changes, and the decrease of transforming growth factor-β signaling pathway. Our findings suggest aging aggravates AAD via 75 miR-1204-MYLK signaling axis.
2024-04-02 | GSE253747 | GEO
Project description:Bicuspid aortic valve (BAV) is the most common congenital heart anomaly and is prone to cause complications, such as valvular stenosis and thoracic aortic dilation. There is currently no reliable way to predict the progression rate to thoracic aortic aneurysm. Here, we aimed to characterize the proteomic landscape in the plasma of stenotic BAV patients and provide potential biomarkers to predict progressive aortic dilation. Plasma samples were obtained from 45 subjects (30 stenotic BAV patients and 15 healthy controls). All samples were properly prepared and analyzed using mass spectrometry (MS)-based label-free quantitative proteomics.
2021-08-19 | PXD027125 | Pride
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 µg/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
Project description:To discover novel biomarkers for aortic aneurysm, serum samples of patients with thoracic aortic aneurysm were fractionated, tryptic digested, and subjected to proteome analysis.
2023-11-15 | PXD033774 | JPOST Repository
Project description:We sought to identify differentially regulated microRNAs in infrarenal mouse aortic tissue after AAA-induction with PPE, compared with sham-operated mice. This treatment leads to rapid development of infrarenal aortic aneurysms with significant diameter differences observed by Day 7. We found 41 miRNAs were up-regulated with aneurysm and 37 down-regulated at p<0.05, which were also altered by >1.5-fold.
2014-08-31 | GSE51226 | GEO
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.
2017-03-31 | MSV000080837 | MassIVE
Project description:Aortic aneurysm is a life-threatening cardiovascular disorder due to the predisposition for dissection and rupture. Genetic studies have proved the involvement of the transforming growth factor-β (TGF-β) pathway in aortic aneurysm. Smad4 is the central mediator of canonical TGF-β signaling. However, the exact role of Smad4 confined to the smooth muscle cells (SMCs) in the pathogenesis of aortic aneurysm is largely unknown. Furthermore, whether TGF-β signaling disruption in SMCs could directly trigger aortic wall inflammation remains poorly investigated. Recently, we revealed a pivotal role of smooth muscle Smad4 signaling in maintaining aortic wall homeostasis and protecting against the development of aortic aneurysm and dissection. To evaluate the underlying mechanism by which Smad4 regulate VSMC functions and affects aneurysm formation and development, Smooth muscle specific Smad4 Knockout mice and the control littermate were sacrificed at 6 weeks old, and their aortic ateries were collected.We combined 3-5 vessels for one sample, and 2 samples for each phenotype. Subsequently, a total of 400ng RNA was used following Affymetrix instruction and 2 ug of cRNA were hybridized for 16 hr at 45°. GeneChips were scanned using the Scanner 7G and the data was analyzed with Expression Console using Affymetrix default analysis settings and global scaling as normalization method. RMA analysis was employed to evaluate the gene expression. We used microarrays to detect the global gene expression in the aortic arteries of smooth muscle cell specific Smad4 knockout mice (Smad4-KO)compared with wild type littermates (WT) at 6 weeks old and identified distinct classes of altered genes.
2016-12-01 | GSE67182 | GEO
Project description:To identify miRNAs which could be involved in TAA (Thoracic Aortic Aneurysm) pathogenesis, we first performed miRNAs microarrays using the aortic media of healthy controls and TAA patients. 473 miRNAs were detected in at least half samples. Among them, 232 miRNAs were differentially expressed with adjusted p value < 0.05 and log2 transformed fold change > 0.5 or < -0.5.
2019-09-18 | GSE110527 | GEO