Proteomic analysis of vesicles derived from ACS patients
Ontology highlight
ABSTRACT:
INSTRUMENT(S):
ORGANISM(S): Homo Sapiens (human)
TISSUE(S): Blood Plasma
DISEASE(S): Cardiovascular System Disease
SUBMITTER: 
Francesca Mensitieri
LAB HEAD: Fabrizio Dal
PROVIDER: PXD059929 | Pride | 2025-09-24
REPOSITORIES: Pride
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| NSTEMI_CAD_EV_a1.raw | Raw | |||
| NSTEMI_CAD_EV_a2.raw | Raw | |||
| NSTEMI_CAD_EV_a3.raw | Raw | |||
| NSTEMI_CAD_EV_a4.raw | Raw | |||
| NSTEMI_CAD_EV_a5.raw | Raw |
Items per page: 5 1 - 5 of 73 |
Similar Datasets
Project description:Background: Acute coronary syndromes (ACS) are associated with aberrant gene expression and epigenetic mechanisms. In particular, de novo DNA methylation is typically linked to gene silencing, but its role in heart disease remains not fully understood. Extracellular vesicles (EVs) are active components in cellular communication for their ability to carry a plethora of signalling biomolecules, thus representing a promising new diagnostic/therapeutic approach in cardiovascular diseases (CVDs). Indeed, there is the need of novel biomarkers for ACS prediction and timely detection. Purpose: We hypothesized that specific epigenetic signals can be carried by EVs. In this regard, we isolated and characterized circulating EVs from ACS patients and evaluated their potential role to influence DNA methylation in target cells. Methods: Circulating EVs were recovered, by ultracentrifugation, from plasma samples of 19 ACS patients and 50 healthy subjects (HS). Nanoparticle tracking analysis (NTA) and western blot (WB) were used to confirm the EVs integrity and purity. Peripheral blood mononuclear cells (PBMCs) of volunteer donors were treated with both ACS and HS derived EVs and genomic DNA was extracted to perform epigenome wide analysis through Reduced Representation Bisulfite Sequencing. ShinyGO, PANTHER, and STRING tools were interrogated to perform GO and PPI network analyses. Flow Cytometry, qRT-PCR, and WB analysis were also performed to evaluate and validate both intra-vesicular and intra-cellular signals. Results: Plasma ACS-derived EVs showed a significant up-regulation of DNA methyltransferases (DNMTs) gene expression levels as compared to HS (P<0.001). Specifically, de novo methylation transcripts, as DNMT3A and DNMT3B were significantly increased in plasma ACS-EVs. DNA methylation analysis of PBMCs from volunteer donors treated with HS- and ACS-derived EVs showed that RNF166 and CCND3 genes resulted the most hyper- and hypo-methylated, respectively, after by ACS-EV treatment. In addition, PPI network analysis specifically evidenced the subnetwork with SRC, as a hub gene, connecting it to NOTCH1, FOXO3, CDC42, IKBKG, RXRA, DGKG, known as important genes already involved in the onset of CVDs. Surprising, other novel genes, BAIAP2, SYP, CHL1, and SHB, which were hypomethylated, were found significantly overexpressed in PBMCs (P<0.005), underlying the fundamental modulating properties of EV cargo in atherosclerosis. Conclusions: These findings support the significant role of ACS plasma-derived EVs, inducing de novo DNA methylation signals, and modulating specific signaling pathways in target cells.
2023-04-03 | E-MTAB-11641 | biostudies-arrayexpress
Project description:Upon activation, platelets release a host of soluble and vesicular signals, collectively termed the ‘platelet releasate’ (PR). The contents of this PR play a significant role in haemostasis, inflammation, and pathologic sequelae. Despite this, proteomic studies investigating the PR in coronary artery disease have not been performed. We undertook a comparative label-free quantitative (LFQ) proteomic profiling of the 1U/ml thrombin-induced PR from 13 acute coronary syndrome (ACS-STEMI) versus 14 stable angina pectoris patients using a tandem mass spectrometry approach. We identified differentially released platet proteins including tetranectin (CLEC3B), protein disulfide-isomerase-A3 (PDIA3), coagulation factor V (F5) and fibronectin (FN1). Strikingly, all 9 differential proteins were associated with the GO cellular component term ‘extracellular vesicle’ and reduced levels of EVs were detected in plasma of ACS-STEMI patients. Network analysis revealed 3 PR proteins either reduced (F5; FN1) or absent (CLEC3B) in ACS-STEMI patients, which are strongly connected to both the clotting cascade and major druggable targets on platelets. This moderated signature highlights the possible basis of platelet dysfunction in ACS-STEMI and may prove useful for non-invasive risk assessment of the progression of coronary artery disease.
2020-06-05 | PXD009356 | Pride
Project description:We have employed whole genome microarray expression profiling as a discovery platform to identify genes involved in plaque rupture. Human coronary artery endothelial cells (ECs) were stimulated in vitro for 12 hours with plasma obtained from the coronary sinus (CS) and the aorta (Ao) of patients with ACS (n=8), or patients with stable angina (SA, n=4). For each patient, gene expression profile was evaluated by microarray technology in ECs exposed to plasma obtained from CS and compared to that of ECs exposed to plasma sampled from Ao. In patient with ACS we found 684 genes up-regulated and 283 down-regulated was observed as compared to patients with SA. Functional and network analyses of statistically significant gene showed that the up regulated genes were associated to pathways IL17 Signaling. To validate the microarray data the RNAs were used for Real Time PCR experiment. Human coronary artery endothelial cells (ECs) were stimulated in vitro for 12 hours with plasma obtained from the coronary sinus (CS) and the aorta (Ao) of patients with ACS (n=8), or patients with stable angina (SA, n=4). For each patient, gene expression profile was evaluated by microarray technology in ECs exposed to plasma obtained from CS and compared to that of ECs exposed to plasma sampled from Ao.
2014-02-14 | E-GEOD-54977 | biostudies-arrayexpress
Project description:Proteome analysis of vesicles of hairy root of Salvia Sclarea by LC-HRMS/MS analysis
2025-05-06 | PXD048610 | Pride
Project description:We aim to determine blood transcriptome-based molecular signature of acute coronary syndrome (ACS), and to identify novel serum biomarkers for early stage ST-segment-elevation myocardial infarction (STEMI) We obtained peripheral blood from the patients with ACS who visited emergency department within 4 hours after the onset of chest pain: a set of blood samples of patients with STEMI (n=7) before and 7 days after the primary percutaneous coronary intervention (n=7) and normal control (n=10)
2015-05-23 | E-GEOD-61144 | biostudies-arrayexpress
Project description:Inflammatory mechanisms and immune cells are involved in acute coronary syndromes (ACS) and may lead to acute plaque rupture. However, the local expression of the different genes potentially involved is largely unknown. We therefore performed an Affymetrix analysis of genes expressed in white blood cells obtained from an occluding coronary thrombus or peripheral blood of patients with ST-elevation myocardial infarction. Thrombi of ACS patients were harvested from the site of coronary occlusion. Leukocytes were isolated by Ficoll centrifugation. Peripheral blood leukocytes (PBL) were treated in a similar fashion and mRNA was extracted from both cells.
2011-12-04 | E-GEOD-19339 | biostudies-arrayexpress
Project description:We aim to determine blood transcriptome-based molecular signature of acute coronary syndrome (ACS), and to identify novel serum biomarkers for early stage ST-segment-elevation myocardial infarction (STEMI) We obtained peripheral blood from the patients with ACS who visited emergency department within 4 hours after the onset of chest pain: ST-elevation myocardial infarction (STEMI, n=7), Non-ST-elevation MI (NSTEMI, n=10) and unstable angina (UA, n=9), and normal control (n=7)
2015-05-23 | E-GEOD-60993 | biostudies-arrayexpress
Project description:We developed a coronary plaque sampling approach that could be applied broadly in live patients with coronary artery disease (CAD) to obtain molecular and cellular insights into human coronary atherosclerosis. Our approach combined RNA retrieval directly from balloons used in percutaneous coronary interventions (PCI) and inexpensive, low-input RNA-Seq using SMART-seq. We generated SMART-Seq libraries from coronary samples from 27 patients. Of the 27 patients, 13 were confirmed to have stable CAD (sCAD) and 14 confirmed to have been performed on lesions causing acute coronary syndrome (ACS). We applied CIBERSORTx to analyze the SMART-seq data from each of the 27 samples. We found fibroblasts and fibromyoctes were enriched, while smooth muscle cells were reduced, in samples from ACS compared with sCAD patients. We identified 371 genes as significantly differential expressed (q<0.05) between sCAD and ACS patients.
2023-07-10 | GSE236610 | GEO
Project description:Coronary artery disease (CAD) remains a leading cause of death worldwide. Acute coronary syndromes (ACS) are the spectrum of diseases arising from coronary atherosclerotic plaque rupture, ranging from unstable angina (UA; clinical symptoms of cardiac ischemia without myocardial necrosis) to myocardial infarction (MI; clinical symptoms of cardiac ischemia with myocardial necrosis). We use microrray to identify changes in pathways following MI.This study examines mRNA expression levels in human whole blood at 7 and 30 days post ACS. Patients with MI are compared to those with UA (not healthy controls), thus focusing on differences in mRNA expression due to the acute clinical events rather than underlying atherosclerosis and its treatment.
2011-05-06 | GSE29111 | GEO
Project description:Currently, it is well established that human endothelial cells (ECs) are characterised by a significant heterogeneity between distinct blood vessels, e.g., arteries, veins, capillaries, and lymphatic vessels. Further, even ECs belonging to the same lineage but grown under different flow patterns (e.g., laminar and oscillatory or turbulent flow) ostensibly have distinct molecular profiles defining their physiological behaviour. Human coronary artery endothelial cells (HCAEC) and human internal thoracic artery endothelial cells (HITAEC) represent two cell lines inhabiting atheroprone and atheroresistant blood vessels (coronary artery and internal thoracic artery, respectively). Resistance of the internal mammary artery to atherosclerosis has been largely attributed to the protective phenotype of HITAEC which reportedly produce higher amounts of vasodilators including nitric oxide (NO) through the respective signaling pathways. However, this hypothesis has not been adequately addressed hitherto as proteomic profiling of HCAEC and HITAEC in a head-to-head comparison setting has not been performed.
2023-10-17 | PXD037861 | Pride