Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

41 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

MicroArray of microRNAs expressed in peripheral blood inflammatory cells from acute myocardial infarction patients. Before and after a primary percutaneous coronary intervention.

ABSTRACT: We studied new microRNAs involved in the left ventricular adverse remodeling (LVAR) process after the ST elevation myocardial infarction (STEMI). We analyzed the expression of miRNAs in peripheral blood mononuclear cells (PBMCs) isolated from a group of non-LVAR (n = 5) and LVAR STEMI patients (n = 5), before (0 hour) and after a primary percutaneous coronary intervention (PPCI; 6 hours).

ORGANISM(S): Homo sapiens

SUBMITTER: Elisa Bevilacqua

PROVIDER: E-MTAB-11002 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Expression data from blood samples of STEMI and Same STEMI patients after PIC

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

Transfer of Alarmins from Neutrophils to Platelets after Acute Myocardial Infarction

Project description:Platelets are central to the pathophysiology of myocardial infarction (MI). How the platelet proteome is altered during MI is unknown. We sought to describe changes in the platelet proteome at the time of MI and identify potential mechanisms. Platelets from patients experiencing ST-elevation myocardial infarction (STEMI) before and 3 days after treatment (n= 30), and a matched cohort of patients with severe stable coronary artery disease(CAD) prior to and 3 days after coronary artery bypass grafting (CABG, n=25) underwent quantitative proteomic analysis. Elevations of the alarmins S100A8 and S100A9 were detected at the time of STEMI compared with stable CAD (S100A8, FC = 2.00, FDR = 0.05; S100A9, FC = 2.28, FDR = 0.005). During STEMI, S100A8 mRNA and protein levels were correlated in platelets (R = 0.46, p = 0.012). To determine if protein synthesis occurs, activated platelets were incubated with 13C-labelled amino acids for 24 hours and analyzed by mass spectrometry. No incorporation was detected, consistent with the notion that protein synthesis in platelets is not a major contributor to the platelet proteome. Platelet abundance of S100A8 and A9 was strongly correlated with neutrophil abundance at the time of STEMI. When isolated platelets and neutrophils were co-incubated under quiescent and TRAP-6 activated conditions, release of S100A8 from neutrophils resulted in uptake of S100A8 by platelets. Leukocyte-to-platelet protein transfer, rather than protein synthesis, may occur in a thromboinflammatory environment such as STEMI, representing a potential new contributor in the innate immune pathogenesis of STEMI.

2023-11-15 | PXD024186 | Pride

Comparative platelet releasate proteome profiling of acute coronary syndrome versus stable coronary artery disease

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

Transfer of Alarmins from Neutrophils to Platelets after Acute Myocardial Infarction

Project description:Platelets are central to the pathophysiology of myocardial infarction (MI). How the platelet proteome is altered during MI is unknown. We sought to describe changes in the platelet proteome at the time of MI and identify potential mechanisms. Platelets from patients experiencing ST-elevation myocardial infarction (STEMI) before and 3 days after treatment (n= 30), and a matched cohort of patients with severe stable coronary artery disease (CAD) prior to and 3 days after coronary artery bypass grafting (CABG, n=25) underwent quantitative proteomic analysis. Elevations of the alarmins S100A8 and S100A9 were detected at the time of STEMI compared with stable CAD (S100A8, FC = 2.00, FDR = 0.05; S100A9, FC = 2.28, FDR = 0.005). During STEMI, S100A8 mRNA and protein levels were correlated in platelets (R = 0.46, p = 0.012). To determine if protein synthesis occurs, activated platelets were incubated with 13C-labelled amino acids for 24 hours and analyzed by mass spectrometry. No incorporation was detected, consistent with the notion that protein synthesis in platelets is not a major contributor to the platelet proteome. Platelet abundance of S100A8 and A9 was strongly correlated with neutrophil abundance at the time of STEMI. When isolated platelets and neutrophils were co-incubated under quiescent and TRAP-6 activated conditions, release of S100A8 from neutrophils resulted in uptake of S100A8 by platelets. Leukocyte-to-platelet protein transfer, rather than protein synthesis, may occur in a thromboinflammatory environment such as STEMI, representing a potential new contributor in the innate immune pathogenesis of STEMI.

2023-11-15 | PXD024159 | Pride

Characterization of the platelet transcriptome by RNA sequencing in patients with acute myocardial infarction.

Project description:Recent technological advances have made transcriptome sequencing (RNA-seq) possible in cells with low RNA copy number including platelets. Resulting studies have used RNA-seq in platelets isolated from healthy individuals to characterize the platelet transcriptome. However, platelets, possibly through gene expression changes, contribute to the etiology of and response to cardiovascular disease and events. To address this, we performed the largest human platelet RNA-seq analysis to date in 34 platelet samples: 16 ST-segment elevation myocardial infarction (STEMI), 16 non-STEMI (NSTEMI), and 2 controls. RNA-seq of platelet samples from 34 individuals: 16 with ST-elevation myocardial infarction (STEMI), 16 with non-STEMI, and 2 non-myocardial infarction controls

2015-09-15 | E-GEOD-65705 | biostudies-arrayexpress

Assessment and Diagnostic Relevance of Novel Serum Biomarkers for Early Decision of ST-elevation Myocardial Infarction

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

Altered gene expression pattern in peripheral blood mononuclear cells in patients with acute myocardial infarction

Project description:Despite a substantial progress in diagnosis and therapy, acute myocardial infarction (MI) is a major cause of mortality in the general population. A novel insight into the pathophysiology of myocardial infarction obtained by studying gene expression should help to discover novel biomarkers of MI and to suggest novel strategies of therapy. The aim of our study was to establish gene expression patterns in leukocytes from acute myocardial infarction patients. ST-segment elevation myocardial infarction alters expression of several groups of genes. On admission, several genes and pathways that could be directly or indirectly linked with lipid/glucose metabolism, platelet function and atherosclerotic plaque stability were affected (signaling of PPAR, IL-10, IL-6). Analysis at discharge highlighted specific immune response (upregulation of immunoglobulins). Highly significant and substantial upregulation of SOCS3 and FAM20 genes expression in the first 4-6 days of myocardial infarction in all patients is the most robust observation of our work Twenty-eight patients with ST-segment elevation myocardial infarction (STEMI) were included. The blood was collected on the 1st day of myocardial infarction, after 4-6 days, and after 6 months. Control group comprised 14 patients with stable coronary artery disease (CAD), without history of myocardial infarction. Gene expression analysis was performed with Affymetrix GeneChipM-BM-. Human Gene 1.0 ST microarrays and GCS3000 TG system.

2014-10-23 | E-GEOD-62646 | biostudies-arrayexpress

Different expression profiles and bioinformatics analysis of circular RNAs between ST-elevation myocardial infarction and chronic artery syndroms.

Project description:We aimed to confirm the different expression profiles of circular RNAs (circRNAs) between ST-elevation myocardial infarction (STEMI) and chronic coronary syndromes (CCS) and identify the role of circRNAs in STEMI.

2022-11-20 | GSE213144 | GEO

Whole blood gene expression profiling for coronary in-stent restenosis: A Indian pilot case study.

Project description:Percutaneous coronary intervention (PCI) with stent placement is a standard treatment for coronary artery disease (CAD). Despite all medical advances, restenosis remains a challenging clinical problem. However, the molecular and biochemical pathways of restenotic process are not fully understood yet. Furthermore, as restenosis is assumed to be a multigenetic process and genetic predisposition is considered an important risk factor, analysis of the genome-wide gene expression is recommended for better insight of the phenomenon. We used microarray technology to monitor thousands of genes expression simultaneously. The whole genome expression will be analyzed with this technique to identify cluster of up-regulated and down-regulated genes which may be involved in this complex pathological condition. Coronary restenosis after percutaneous coronary intervention remains a challenging problem, despite all medical advances. Molecular and biochemical pathways of restenotic process are not fully understood yet. Furthermore, as restenosis is assumed to be a multigenetic process. We used microarray technology to monitor thousands of genes expression simultaneously in restenosis postive group with reference restenosis negative group, which will unravel potentially modifiable pathways, possible targets and biomarkers for coronary restenosis.

2014-04-30 | E-GEOD-46560 | biostudies-arrayexpress

Characterization of the platelet transcriptome by RNA sequencing in patients with acute myocardial infarction.

2015-09-15 | GSE65705 | GEO