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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE252397 | GEO | 2024/03/21

REPOSITORIES: GEO

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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

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

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

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

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

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

Identification of common lupus-disease related microRNA expression pattern in three different murine models of lupus

Project description:In this study, miRNA expression in splenic lymphocytes from three genetically disparate lupus-prone mouse models (MRL-lpr, B6-lpr and NZB/WF1) were profiled. 49 miRNAs were found to be differentially expressed in MRL-lpr mice compared to MRL mice; and 24 miRNAs were differentially expressed in B6-lpr mice compared to B6 mice. Among these dysregulated miRNAs, we noted that 15 miRNAs were common to both lpr strains. Interestingly, microarray analysis of NZB/W and NZW at 3 months of age, an age when overt lupus disease is not evident in NZB/W mice, revealed that only one miRNA, miR-148a was significantly upregulated in NZB/W mice. The aim of this porject is to determine the common miRNA expression changes in splenocytes from different strains of murine lupus models. The splenocytes were prepared from genetically lupus-prone female mice including MRL/MpJ-Faslpr/J (MRL-lpr), NZBWF1/J (NZB/W), B6.MRL-Faslpr/J (B6-lpr) and their control mice MRL/MpJ (MRL), NZW/LacJ (NZW) and C57BL/6J (B6) mice (The Jackson laboratory, ME). Total RNAs, containing miRNAs were isolated from whole splenocytes using mirVana miRNA isolation kits (Ambion) following manufactory’s instructions and sent to LC Sciences (http://www.lcsciences.com/) for the microarray assay. The mouse miRNA array chips (Chip ID miRMouse 12.0 version), which included 617 unique, mature, mouse miRNA, based on the Sanger miRBase Release 12.0, were used in the assay.

2011-12-17 | E-GEOD-22359 | biostudies-arrayexpress

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

Identification of common lupus-disease related microRNA expression pattern in three different murine models of lupus

2011-12-17 | GSE22359 | 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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