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Genome-wide DNA methylation analysis in primary antiphospholipid syndrome neutrophils

ABSTRACT: Genome-wide DNA methylation analysis in primary antiphospholipid syndrome neutrophils

PROVIDER: PRJNA512512 | ENA |

REPOSITORIES: ENA

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Genome-wide DNA methylation analysis in primary antiphospholipid syndrome neutrophils

2019-01-02 | GSE124565 | GEO

RNA-Seq in neutrophils from Antiphospholipid Syndrome

Project description:Antiphospholipid antibodies are a leading cause of thrombosis. To further elucidate the role of neutrophils in APS, we performed a comprehensive transcriptome analysis using the total RNA of neutrophils isolated from 9 patients with primary APS and 9 age, sex and ethnicity-matched healthy controls using next-generation RNA-seq.

2017-11-15 | GSE102215 | 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

Genome-wide DNA methylation analysis in primary antiphospholipid syndrome neutrophils.

Project description:Antiphospholipid syndrome (APS) is a systemic autoimmune disease characterized by thromboembolic events and pregnancy loss. We sought to characterize the DNA methylation profile of primary APS in comparison to healthy controls and individuals with SLE. In primary APS neutrophils compared to controls, 17 hypomethylated and 25 hypermethylated CpG sites were identified. Notable hypomethylated genes included ETS1, a genetic risk locus for SLE, and PTPN2, a genetic risk locus for other autoimmune diseases. Gene ontology analysis of hypomethylated genes revealed enrichment of genes involved in pregnancy. None of the differentially methylated sites in primary APS were differentially methylated in SLE neutrophils, and there was no demethylation of interferon signature genes in primary APS as is seen in SLE. Hypomethylation within a single probe in the IFI44L promoter (cg06872964) was able to distinguish SLE from primary APS with a sensitivity of 93.3% and specificity of 80.0% at a methylation fraction of 0.329.

| S-EPMC6413498 | biostudies-literature

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

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

RNA sequencing of primary Sjögren’s syndrome neutrophils

Project description:RNA sequencing of primary Sjögren’s syndrome neutrophils

| PRJNA799777 | ENA

B cells in triple positive antiphospholipid syndrome

Project description:B cells in triple positive antiphospholipid syndrome

| PRJNA1090881 | ENA

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

RNA sequencing of primary Sjögren’s syndrome neutrophils

Project description:Objective Neutrophils and aberrant NETosis have been implicated in the pathogenesis of diverse autoimmune diseases, however, their roles in primary Sjögren’s syndrome (pSS) remain unclear. We aimed to reveal the potential roles of neutrophils and neutrophil extracellular traps (NETs) in this study. Methods pSS patients were enrolled according to the corresponding diagnostic criteria. NETosis markers were measured in plasma and small salivary gland using ELISA and immunofluorescence. The gene signatures of neutrophils were assessed by RNA-Seq and RT-PCR. Reactive oxygen species (ROS), mitochondrial ROS (mitoROS) production and JC-1 was measured by flow cytometry. Results NETosis markers including cell free-DNA (cf-DNA), myeloperoxidase (MPO) in plasma and small salivary gland from pSS patients were significantly higher than healthy controls (HCs) and were associated with disease activity. RNA sequencing and RT-qPCR revealed activated Type I IFN signaling pathway and higher expression of type I interferon related genes in pSS neutrophils. Further stimulating with IFN-α 2a in vitro significantly induced ROS production and JC-1 monomer percentage in pSS neutrophils. Conclusions Our data suggest the involvement of neutrophils and enhanced NETosis in pSS patients. Further mechanism study in vitro revealed that type I IFN activation in pSS neutrophils led to mitochondrial damage and related ROS production which finally result in the generation of NETs.

2022-01-25 | GSE194234 | GEO

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