Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

MiRNAs screening in small extracellular vesicles (sEVs) from patients with primary antiphospholipid syndrome (PAPS)

ABSTRACT: To discover miRNAs implicate in PAPS pathogenesis, we isolated sEVs from plasma of PAPS patients, aPL patients (patients with positive antiphospholipid antibodies without thrombotic or obstretic complications) and control. Then, we extracted RNA total and we performed miRNA-sequencing.

ORGANISM(S): Homo sapiens

PROVIDER: GSE220791 | GEO | 2023/07/18

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

miRNAs screening in small extracellular vesicles (sEVs) from patients with primary antiphospholipid syndrome (PAPS)

Project description:miRNAs screening in small extracellular vesicles (sEVs) from patients with primary antiphospholipid syndrome (PAPS)

| PRJNA911334 | ENA

B cells in triple positive antiphospholipid syndrome

Project description:Peripheral B cell selection of autoreactive B cells is crucial for preventing autoimmunity. In this study, we identify that a significant proportion of antiphospholipid (aPL) B cells present in the naive compartment, exhibit polyreactivity and belong to the natural repertoire. We used scRNA Seq to follow B cells with aPL features throughout their development from naïve B cells to plasma cells in patients with PAPS.

2024-10-08 | GSE262240 | GEO

Gene profiling reveals specific molecular pathways in the pathogenesis of atherothrombosis in Antiphospholipid syndrome, Systemic Lupus Erythematosus and Lupus with Antiphospholipid Syndrome

2014-03-12 | GSE50395 | GEO

Gene expression profile in human monocytes treated with IgG from APS patients or IgG from controls

Project description:The antiphospholipid syndrome (APS) is an autoimmune disease in which antiphospholipid antibodies (aPL) cause vascular thrombosis (VT+) and/or pregnancy morbidity (PM+). The experiment aimed at determining whether specific aPL are associated with thrombotic or obstetric manifestations. In the present study we carried out microarray analysis comparing patterns of mRNA expression in monocytes from a healthy volunteer exposed to IgG from patients with a history of vascular thrombosis (VT+/PM-) or pregnancy morbidity (VT-/PM+) or to IgG from healthy controls (HC).

2018-04-28 | E-MTAB-6671 | biostudies-arrayexpress

Targeting the tissue factor coagulation initiation complex prevents antiphospholipid antibody development

Project description:Antiphospholipid antibodies (aPL) in primary or secondary antiphospholipid syndrome (APS) areis a major cause for acquired thrombophilia. Here we test the effect of specific inhibition of the TF coagulation initiation complex with nematode anticoagulant protein c2 (NAPc2) on the activation of monocytes by aPL. NGS data show that aPL-induced proinflammatory and prothrombotic activation of monocytes, but not interferon regulated gene induction is prevent by NAPc2.

2024-03-21 | GSE252972 | GEO

Whole blood transcriptome identifies interferon-regulated genes as key drivers in thrombotic primary antiphospholipid syndrome

Project description:Objective: Pathogenesis of antiphospholipid syndrome (APS) isn't fully elucidated. We aimed to identify gene signatures characterizing thrombotic primary APS (thrPAPS) and subgroups at high risk for worse outcomes. Methods: We performed whole blood next-generation RNA-sequencing in 62 patients with thrPAPS and 29 age-/sex-matched healthy controls (HCs), followed by differential gene expression analysis (DGEA) and enrichment analysis. We trained models on transcriptomics data using machine learning. Results: DGEA of 12.306 genes revealed 34 deregulated genes in thrPAPS versus HCs; 33 were upregulated by at least 2-fold, and 14/33 were type I and II interferon-regulated genes (IRGs) as determined by interferome database. Machine learning applied to deregulated genes returned 79% accuracy to discriminate thrPAPS from HCs, which increased to 82% when only the most informative IRGs were analyzed. Comparison of thrPAPS subgroups versus HCs showed an increased presence of IRGs among upregulated genes in venous thrombosis (21/23, 91%), triple-antiphospholipid antibody (aPL) positive (30/50, 60%), and recurrent thrombosis (19/42, 45%) subgroups. Enrichment analysis of upregulated genes in triple-aPL positive patients revealed terms related to 'type I interferon signaling pathway' and 'innate immune response'. DGEA among thrPAPS subgroups revealed upregulated genes, including IRGs, in patients with venous versus arterial thrombosis (n = 11, 9 IRGs), triple-aPL versus non-triple aPL (n = 10, 9 IRGs), and recurrent versus non-recurrent thrombosis (n = 10, 3 IRGs). Conclusion: Upregulated IRGs may better discriminate thrPAPS from HCs than all deregulated genes in peripheral blood. Taken together with DGEA data, IRGs are highly expressed in thrPAPS and high-risk subgroups of triple-aPL and recurrent thrombosis, with potential treatment implications.

2023-12-15 | GSE205465 | GEO

Gene profiling reveals specific molecular pathways in the pathogenesis of atherothrombosis in Antiphospholipid syndrome, Systemic Lupus Erythematosus and Lupus with Antiphospholipid Syndrome

Project description:The present gene expression array study of comparative gene profile in monocytes from patients with primary Antiphospholipid Syndrome, Systemic Lupus Erythematosus and Lupus with Antiphospholipid Syndrome demonstrates that the gene expression profiling allows the segregation of these highly related autoimmune diseases, with specific signatures explaining the pro-atherosclerotic, pro-thrombotic and inflammatory changes. One hundred and twenty six patients, forty one with APS, thirty one with SAPS and fifty four with SLE, as well as sixty one healthy donors were included in the study. Monocytes were purified from peripheral blood samples (non-monocytes depleting kit, Miltenyi Biotech, Bergisch Galdbach, Germany). Total RNA from monocytes was extracted using TRIzol reagent. RNA quality control was performed in a 2100 Bioanalyzer. Complementary RNAs from 3 APS patients, 3 SAPS patients, 3 SLE patients, and 3 healthy donors were prepared for hybridization in an Agilent G4112F platform (Whole human Genome microarray 44K) using the One-color gene expression system (Agilent technologies).

2014-03-12 | E-GEOD-50395 | biostudies-arrayexpress

Transcriptome profiling of PBMCs from primary antiphospholipid syndrome and systemic lupus erythematosus patients and healthy controls

Project description:explore the transcriptome profiles of PBMCs derived from individuals with Primary antiphospholipid syndrome (PAPS) and compared<br>them with those of healthy individuals. Also compare the transcriptome profiles of the closely related Systemic lupus Erythematosus autoimmune disorder with the same profiles from healthy individuals

2008-06-27 | E-MEXP-1635 | biostudies-arrayexpress

Targeting the tissue factor coagulation initiation complex prevents antiphospholipid antibody development.

Project description:Antiphospholipid antibodies (aPL) in primary or secondary antiphospholipid syndrome (APS) are a major cause for acquired thrombophilia. Here we show that specific inhibition of the TF coagulation initiation complex with nematode anticoagulant protein c2 (NAPc2) prevents the the development of persistent aPL and circulating phospholipid-reactive B1 cells in latent viral infection and lupus prone MRL-lpr mice. NGS mRNA profiling of splenic DC in lupus mice treated with NAPc2 versus saline control uncovered a suppression of dendritic cell activation in the spleen.

2024-03-21 | GSE252397 | GEO

Antiphospholipid antibodies induce Proinflammatory and Procoagulant Pathways in Endothelial cells.

Project description:Antiphospholipid syndrome (APS) is an autoimmune thrombophillia characterized by recurrent thrombotic events and/or pregnancy morbidity in the presence of antiphospholipid antibodies detected either as anti-cardiolipin, anti-β2 Glycoprotein I (anti-β2GPI) or Lupus anticoagulant (LA). Endothelial deregulation characterizes the syndrome. To address the gene expression changes occurring in the endothelial cells in the context of APS, we performed transcriptome analysis of Human Umbilical Vein Endothelial cells (HUVECs) stimulated with anti-β2GPI-β2GPI complexes.

2023-05-24 | GSE143506 | 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