Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

GP IIb/IIIa-ICAM-1 Mediated Platelet-Endothelial Adhesion Exacerbates Pulmonary Hypertension

ABSTRACT: Pulmonary hypertension (PH) patients typically present with a diminished platelet count, but the role of platelets in the development and progression of PH remains unclear.Transcriptomic analysis revealed that platelets from PH patients exhibited an upregulation of genes associated with cellular adhesion, platelet activation, and adhesion. Notably, the hub genes, glycoprotein IIb/IIIa (GP IIb/IIIa), were implicated in mediating platelet-endothelium adhesion through their interaction with intercellular adhesion molecule-1 (ICAM-1) on pulmonary artery endothelial cells, triggering platelet activation and the subsequent release of platelet-derived growth factor BB (PDGF-BB).

ORGANISM(S): Homo sapiens

PROVIDER: GSE283520 | GEO | 2024/12/09

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

GP IIb/IIIa-ICAM-1 Mediated Platelet-Endothelial Adhesion Exacerbates Pulmonary Hypertension

Project description:GP IIb/IIIa-ICAM-1 Mediated Platelet-Endothelial Adhesion Exacerbates Pulmonary Hypertension

| PRJNA1194190 | ENA

New alterations of the platelet proteome in type I Glanzmann thrombasthenia

Project description:The project contains raw and result files of a proteomics analysis of two patients with type 1 Glanzmann thrombasthenia (Patient1 and 2) caused by homozygous ITGA2b delG mutations and from family (heterozygous: Father1, Mother1, Sister1, healthy: Sister2) and unrelated controls. A label-free analysis has been conducted in duplicates using Progenesis (NonLinear Dynamics) demonstrating that less than 5% of glycoprotein IIb and 5-7% fibrinogen is expressed compared to healthy controls. Heterozygous familiy members from one of the controls expressed 50-60% of GPIIb sufficient for normal GPIIb/IIIa-dependant platelet function. In a subsequent targeted LC-MS/MS analysis we quantified 14 protein identified as potentially regulated in preliminary iTRAQ experiments. We observed diminished expession of factor XIIIB chain (P05160), plasminogen (P00747) and carboxypeptidase 2B (Q96IY4) in thrombasthenic platelets as well as a 2.5-fold increased expression of FcgRIIA (P12318/P31995) and laminin alpha4 (Q16363).

2019-01-14 | PXD003912 | Pride

Transcriptome profiling of purified mouse platelets from Nxf1 mutant and control mice [Platelet]

Project description:Purpose: Nxf1 is thought to be an essential nuclear exporter of messenger RNA (mRNA) in eukaryotic cells. Whether perturbations in the Nxf1 pathway affect mammalian physiology is not known. The aim of this study is to determine the impact of a Nxf1 mutation in the representation of mRNA transcripts in platelets. Methods: Platelets were purified from individual males. Blood was obtained by cardiac puncture into 0.1 volume of Aster Jandl citrate-based anticoagulant. Mouse platelet rich fraction was obtained by centrifugation of the murine blood at 125 g for 8 min at room temperature, followed by centrifugation of the supernatant buffy coat at 125 g for 8 min. Mouse platelets were washed by two sequential centrifugations at 860 g for 5 min in 140 mM NaCl, 5 mM KCl, 12 mM trisodium citrate, 10 mM glucose, and 12.5 mM sucrose, pH 6.0.The platelet pellet was resuspended in 10 mM Hepes, 140 Mm NaCl, 3 mM KCl, 0.5 mM MgCl2, 10 mM glucose, and 0.5 mM NaHCO3, pH 7.4. The purity of each platelet suspension was assessed by flow cytometry and suspensions for which more than 98% of total events were CD41+ platelets were pooled together. RNA was purified with Norgen cytoplasmic and nuclear fractionation RNA purification kit.

2020-03-04 | GSE141159 | 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

Platelet-secreted microRNA-223 promotes endothelial cell apoptosis induced by advanced glycation end products via targeting the insulin-like growth factor 1 receptor

Project description:Platelets contain abundant miRNAs, however, the biogenesis pathway of miRNAs in anucleate platelets is unclear. Platelet-rich plasma was diluted in washing buffer and the platelet suspension was centrifuged to isolated pure platelets.Finally, platelets were recovered in suspension buffer at the concentration of 4–5×10^8 platelets/ml. Aliquots of the platelet suspensions were activated in the presence of 2.5 mM CaCl2 with 0ng/ml or 1 ng/ml thrombopoietin (TPO)

2014-02-04 | E-GEOD-51453 | biostudies-arrayexpress

Platelet microRNA expression profiles of acute coronary syndrome patients with high and low platelet reactivity

Project description:To explore the diverse platelet microRNA (miRNA) expression between high platelet reactivity (HPR) and low platelet reactivity (LPR) patients with acute coronary syndromes (ACS), we enrolled a cohort of ACS patients and performed miRNA expression profiling of platelets from four HPR and four LPR patients using human miRNA microarray system. VerifyNow P2Y12 assay was applied to indentify HPR and LPR. Venous blood was drawn from the patients and was centrifuged to prepare platelets. Among the candidate differentially expressed miRNAs, miR-15b expression was further confirmed to be lower in platelets of 22 HPR patients than 17 LPR by quantitative reverse-transcription polymerase chain reaction (RT-qPCR). We enrolled a consecutive cohort of 290 ACS patients and assessed the platelet reactivity using VerifyNow P2Y12 assay. In this study, HPR was defined as M-bM-^IM-%300 platelet reactivity unit (PRU) while LPR <170 PRU. miRNA microarray analysis was performed in platelets of four HPR and four LPR patients with ACS.

2014-07-17 | E-GEOD-59488 | biostudies-arrayexpress

eMERGE III: CCHMC - eMERGE Cohorts - Phase IIIA

Project description:eMERGE III: CCHMC - eMERGE Cohorts - Phase IIIA

| PRJNA299710 | ENA

Platelet microRNA-mRNA Co-Expression Profiles Correlate with Platelet Reactivity

Project description:MicroRNAs (miRNAs) regulate cell physiology by altering protein expression, but the biology of platelet miRNAs is largely unexplored. We tested whether platelet miRNA levels were associated with platelet reactivity by genome-wide profiling using platelet RNA from 19 healthy subjects. We found that human platelets express 284 miRNAs. Unsupervised hierarchical clustering of miRNA profiles resulted in 2 groups of subjects that appeared to cluster by platelet aggregation phenotypes. Seventy-four miRNAs were differentially expressed (DE) between subjects grouped according to platelet aggregation to epinephrine, a subset of which predicted the platelet reactivity response. Using whole genome mRNA expression data on these same subjects, we computationally generated a high-priority list of miRNA-mRNA pairs in which the DE platelet miRNAs had binding sites in 3'UTRs of DE mRNAs, and the levels were negatively correlated. Three miRNA-mRNA pairs (miR-200b:PRKAR2B, miR-495:KLHL5 and miR-107:CLOCK) were selected from this list and all 3 miRNAs knocked down protein expression from the target mRNA. Reduced activation from platelets lacking PRKAR2B supported these findings. In summary, (1) platelet miRNAs are able to repress expression of platelet proteins, (2) miRNA profiles are associated with and may predict platelet reactivity, and (3) bioinformatic approaches can successfully identify functional miRNAs in platelets. Total RNA from the platelets of 19 donors was harvested and labeled with Hy3. Reference RNA (a pool of all samples) was labeled with Hy5. This submission represents the miRNA expression component of the study.

2011-09-26 | E-GEOD-27917 | biostudies-arrayexpress

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

Transcriptional impairments in mouse model of mucopolysaccharidosis IIIA and responses to systemic gene delivery using adeno-associated virus serotype rh74 vector (AAVrh74)

Project description:Mucopolysaccharidosis (MPS) IIIA is a neuropathic lysosomal storage disease caused by deficiency in SGSH. Genome-wide gene expression microarrays in MPS IIIA mice detected broad molecular abnormalities (≥2 fold, FDR≤10) in numerous transcripts (314) in the brain and blood (397). Importantly, 22 dysregulated blood transcripts are known to be enriched in the brain and linked to broad neuronal functions. To target the root cause, we used a self-complementary (sc) AAVrh74 vector to deliver the human SGSH gene into 4-6-wk-old MPS IIIA mice by an intravenous injection. The treatment resulted in global CNS and widespread somatic restoration of SGSH activity, clearance of CNS and somatic GAG storage, improved behavior performance, and significantly extended survival. The scAAVrh74-hSGSH treatment also led to the correction of the majority of the transcriptional abnormalities in the brain (95.9%) and blood (97.7%), of which 182 and 290 transcripts were normalized in the brain and blood, respectively. These results demonstrate that a single systemic scAAVrh74-hSGSH delivery mediated efficient restoration of SGSH activity and resulted in a near complete correction of MPS IIIA molecular pathology. This study also demonstrates that blood transcriptional profiles reflect the biopathological status of MPS IIIA, and also respond well to effective treatments.

2017-04-14 | GSE97759 | GEO

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