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Genetics of Antiphospholipid Antibody Syndrome (APS) - RTDC 5806

ABSTRACT: Genetics of Antiphospholipid Antibody Syndrome (APS) - RTDC 5806

PROVIDER: PRJNA497168 | ENA |

REPOSITORIES: ENA

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Genetics of Antiphospholipid Antibody Syndrome (APS) - RTDC 5806

Project description:Genetics of Antiphospholipid Antibody Syndrome (APS) - RTDC 5806

| PRJNA497167 | ENA

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.

2019-01-02 | GSE124565 | 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

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

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

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

A serum nuclear magnetic resonance-based metabolomic signature of antiphospholipid syndrome

Project description:Antiphospholipid syndrome (APS) is a rheumatic inflammatory chronic autoimmune disease inducing hypercoagulable state associated with vascular thrombosis and pregnancy loss in women. Cardiac, cerebral and vascular strokes in these patients are responsible for reduction in life expectancy. Timely diagnosis and accurate monitoring of disease are decisive to improve the accuracy of therapy. In the present work, we present a NMR-based metabolomic study of blood sera of APS patients. Our data show that individuals suffering APS have a characteristic metabolomic profile with abnormalities associated to the metabolism of methyl group donors, ketone bodies and amino acids. We have identified for the first time the metabolomic fingerprint characterizing APS disease having potential application to improve APS timely diagnosis and appropriate therapeutic approaches.

2017-09-06 | MTBLS356 | MetaboLights

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

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