Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Platelet proteomics reveals mechanism of platelet activation inhibition by AEE

ABSTRACT: A platelet proteomic approach to reveal the regulatory network by which AEE inhibits platelet activation, thereby preventing thrombosis.

ORGANISM(S): Rattus Rattus

SUBMITTER: Yajun Yang

PROVIDER: PXD054906 | iProX | Wed Aug 14 00:00:00 BST 2024

REPOSITORIES: iProX

ACCESS DATA

Json Xml

Publications

Platelet Proteomics and Tissue Metabolomics Investigation for the Mechanism of Aspirin Eugenol Ester on Preventive Thrombosis Mechanism in a Rat Thrombosis Model.

Tao Qi Q Fan Li-Ping LP Feng Ji J Zhang Zhi-Jie ZJ Liu Xi-Wang XW Qin Zhe Z Li Jian-Yong JY Yang Ya-Jun YJ

International journal of molecular sciences 20241006 19

Platelet activation is closely related to thrombosis. Aspirin eugenol ester (AEE) is a novel medicinal compound synthesized by esterifying aspirin with eugenol using the pro-drug principle. Pharmacological and pharmacodynamic experiments showed that AEE has excellent anti-inflammatory, antioxidant, and inhibitory platelet activation effects, preventing thrombosis. However, the regulatory network and action target of AEE in inhibiting platelet activation remain unknown. This study aimed to invest ...[more]

PMID: 39409077

Similar Datasets

Prevention of acute thrombosis with vascular endothelium antioxidative nanoscavenger

Project description:Antiplatelet drugs have represented a milestone in treating patients at high risk of thrombosis. However, their clinical use remains limited by bleeding-associated risk and limited efficacy. Excessive reactive oxygen species (ROS) produced by damaged vascular endothelial cells, have been shown to stimulate thrombosis. Here, we propose that a ROS-chemotactic nanoscavenger (MDCP), formed by crosslinking melanin and catalase, prevents acute thrombosis by protecting vascular endothelial cells from oxidative stress. We demonstrate that treatment with MDCP inhibits ROS-induced apoptosis of endothelial cells, thereby maintaining endothelial integrity and preventing collagen exposure, which consequently prevents platelet activation and thrombosis. By avoiding direct interference with platelet function, this modulation of vascular redox homeostasis via MDCP provides a promising alternative antithrombotic strategy that addresses the bleeding risk of current clinical antithrombotic drugs.

2025-11-30 | GSE307563 | GEO

Platelet gene expression profiling of acute myocardial infarction

Project description:Acute myocardial infarction (AMI) is primarily due to coronary atherosclerotic plaque rupture and subsequent thrombus formation. Platelets play a key role in the genesis and progression of both atherosclerosis and thrombosis. Since platelets are anuclear cells that inherit their mRNA from megakaryocyte precursors and maintain it unchanged during their life span, gene expression (GE) profiling at the time of an AMI provides information concerning the platelet GE preceding the coronary event. In ST-segment elevation myocardial infarction (STEMI), a gene-by-gene analysis of the platelet GE identified five differentially expressed genes (DEGs): FKBP5, S100P, SAMSN1, CLEC4E and S100A12. The logistic regression model used to combine the GE in a STEMI vs healthy donors score showed an AUC of 0.95. The same five DEGs were externally validated using platelet GE data from patients with coronary atherosclerosis but without thrombosis. Early signals of an imminent AMI are likely to be found by platelet GE profiling before the infarction occurs.

2019-12-31 | GSE109048 | GEO

Prostate cancer cell-platelet bidirectional signaling promotes calcium mobilization, invasion and apoptotic resistance via distinct receptor-ligand pairs

Project description:Platelets play a crucial role in cancer and thrombosis. The receptor-ligand repertoire mediating prostate cancer (PCa) cell-platelet interactions have not been fully elucidated. Microvilli emanating from the plasma membrane of PCa cell lines (RC77 T/E, MDA PCa 2b) directly contacted individual platelets and platelet aggregates, thereby stimulating calcium mobilization in platelets and promoting translocation of P-selectin and integrin aIIbb3 onto the platelet surface. Platelets in turn dose-dependently stimulated PCa cell invasion and apoptotic resistance. PCa cells were exceedingly sensitive to activation by platelets, occurring at platelet:PCa cell ratios ~20,000-fold lower than normally encountered in blood. Candidate platelet-PCa cell signaling axis partners responsible for these cellular events were identified by RNA-Seq and could be broadly divided into 4 categories: i) integrin-ligand, ii) EPH receptor-ephrin, iii) immune checkpoint receptor-ligand, and iv) miscellaneous receptor-ligand interactions. PCa cell-stimulated calcium mobilization was mediated by a fibronectin1 (FN1; PCa side)-aIIbb3 (platelet side) axis. Reciprocally, platelet-stimulated PCa cell invasion was facilitated by a CD55 (platelet side)-adhesion G-protein coupled receptor E5 (ADGRE5; PCa side) axis, with contribution from platelet cytokines CCL3L1 and IL32. Platelet-stimulated PCa cell apoptotic resistance relied on ephrin-EPH receptor and lysophosphatidic acid (LPA)-LPA receptor (LPAR) signaling. Of the participating partners, FN1 and LPAR3 overexpression was observed in PCa specimens compared to normal prostate, while high expression of CCR1 (CCL3L1 receptor), EPHA1 and LPAR5 in PCa was associated with poor patient survival. These findings emphasize that non-overlapping receptor-ligand pairs participate in oncogenesis and thrombosis, highlighting the complexity of any contemplated clinical intervention strategy.

2022-11-05 | GSE216942 | GEO

Towards a reference human platelet transcriptome: evaluation of inter-individual correlations and of its relationship with a platelet proteome

Project description:For the anucleate platelet it has been unclear how well platelet transcriptomes correlate among different donors or across different RNA profiling platforms, and what the transcriptomes’ relationship is with the platelet proteome. We generated RNA-seq pro-files of the long RNA transcriptomes from the platelets of 10 healthy young males (5 white and 5 black) with median age of 24.5 years, no notable clinical history, and no pre-vious history of thrombosis or bleeding. We also profiled the subjects’ messenger RNAs using the Affymetrix microarray gene expression system. We found that the abundance of platelet mRNA transcripts was highly correlated across the 10 individuals, inde-pendently of race and of the employed technology. Our RNA-seq data also showed that these high inter-individual correlations extend beyond mRNAs to several categories of non-coding RNAs. Pseudogenes represented a notable exception to this by exhibiting a clear difference in expression by race. Comparison of our mRNA signatures with the only publicly available quantitative platelet proteome data showed that most (87.5%) identified platelet proteins had a detectable corresponding mRNA. However, a high number of mRNAs that were present in the transcriptomes of all 10 individuals had no representa-tion in the proteome. The Spearman correlation of the relative abundances for those platelet genes that were represented by both an mRNA and a protein showed a weak (~0.3) yet statistically significant (P=5.0E-16) connection. Further analysis of the overlap-ping and non-overlapping platelet mRNAs and proteins identified gene groups corre-sponding to distinct cellular processes, a finding that provides novel insights for platelet biology. This represents the Affymetrix GeneChip component of the study only 10 Resting Human Platelet samples

2015-01-20 | E-GEOD-50858 | biostudies-arrayexpress

TNFα Downregulates STX17 Blocking Autophagy and Impairing Platelet Metabolism and Clot Contraction

Project description:Platelets are key players in hemostasis and thrombosis. In inflammatory conditions, platelets are hyperreactive and patients have an overal increased thrombotic risk. Our previous research demonstrated that TNFα significantly increases mitochondrial mass and platelet reactivity, emphasizing the crucial role of TNFα in modulating platelet metabolism and function.We hypothesized that TNFα disrupts platelet metabolism and function by inhibiting autophagy and mitophagy, which are critical processes for preserving mitochondrial mass, integrity, and energy production. We investigated the function, metabolism, and autophagy of human and mouse platelets in myeloproliferative neoplasms, rheumatoid arthritis, and aseptic inflammation. Our analysis reveled a blocked

2025-03-31 | GSE282993 | GEO

MTH1's role in platelet function

Project description:MTH1 knockout mice were utilized to evaluate its role in platelet mitochondrial function and thrombosis

2023-04-14 | PXD041528 |

platelet hyperreactivity project

Project description:The aim of this study is to identify candidate genes modulating platelet reactivity in aspirin-treated cardiovascular patients using an integrative network-based approach. Platelet reactivity was assessed in 110 cardiovascular patients treated with aspirin 100mg/d by aggregometry using several agonists. Patients with extreme high or low PR were selected for further analysis. Data derived from quantitative proteomic of platelets and platelet sub-cellular fractions, as well as from transcriptomic analysis were integrated with a network biology approach.

2019-03-14 | MSV000083572 | MassIVE

Platelet Activation and a Platelet Biosignature Associates with Enhanced Cardiovascular Risk in Patients with Controlled Psoriasis.

Project description:The underlying mechanisms of atherosclerosis and strategies identifying high cardiovascular (CV) risk in psoriasis are incompletely understood. Platelet activity is increased in psoriasis and induces vascular dysfunction. We investigated the platelet phenotype and platelet transcriptome as one potential mechanism to explain CV risk in psoriasis. Psoriasis and controls underwent platelet aggregation and activation studies and platelet RNA sequencing to generate a psoriasis platelet transcriptomic score. The relationship between the platelet transcriptomic score and CV risk was assessed by arterial stiffness, coronary calcium, and longitudinally in an independent cohort of high CV-risk individuals undergoing lower extremity arterial revascularization (LER).

2025-09-08 | GSE302674 | GEO

Towards a reference human platelet transcriptome: evaluation of inter-individual correlations and of its relationship with a platelet proteome

2015-01-20 | GSE50858 | GEO

Platelet Proteome in Myeloproliferative Neoplasms

Project description:Patients with chronic Myeloproliferative Neoplasms (MPN) including polycythaemia vera (PV) and essential thrombocythemia (ET) exhibit unique clinical features, such as a tendency toward thrombosis and hemorrhage, and risk of disease progression to secondary bone marrow fibrosis and/or acute leukemia. Although an increase in blood cell lineage counts (quantitative features) contribute to these morbid sequelae, the significant qualitative abnormalities of myeloid cells that contribute to vascular risk are not well understood. Here, we address this critical knowledge gap via a comprehensive and untargeted profiling (using label free quantitative mass spectrometry) of the platelet proteome in a large (n= 140) cohort of patients (from two independent sites) with an established diagnosis of PV and ET. We discover distinct MPN platelet protein expression and confirm key molecular impairments associated with proteostasis and thrombosis mechanisms of potential relevance to MPN pathology.

2024-10-17 | PXD046324 | Pride

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