ABSTRACT: 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.
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
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).
Project description:Autoantibodies target the RNA-binding protein Ro60 in systemic lupus erythematosus (SLE) and Sjögren's syndrome. However, whether Ro60 and its associated RNAs contribute to disease pathogenesis is unclear. We catalogued the Ro60-associated RNAs in human cell lines. iCLIP in 2 cell lines (GM12878, K562).
Project description:Autoantibodies target the RNA-binding protein Ro60 in systemic lupus erythematosus (SLE) and Sjögren's syndrome. However, whether Ro60 and its associated RNAs contribute to disease pathogenesis is unclear. We catalogued the Ro60-associated RNAs in human cell lines.
Project description:The molecular basis for the female bias of systemic lupus erythematosus remains unclear. We sought to determine the fidelity of dynamic X-chromosome inactivation maintenance in the pathogenesis of murine models of spontaneous lupus, including the heavily female-biased NZM2328 model.
Project description:We performed spatial transcriptomics on a case series of different clinical subtypes of cutaneous lupus erythematosus including acute cutaneous lupus erythematosus (malar rash, systemic lupus erythematosus). Our goals were to (1) determine which differentially expressed genes (DEGs) could be attributed to specific cell populations in specific locations within the tissue, (2) determine if spatial transcriptomics could better distinguish between CLE clinical subtypes than bulk RNA approaches and (3) examine potential cell-cell communication pathways within the skin lesions.
Project description:T-cells are important in the pathogenesis of juvenile-onset systemic lupus erythematosus (JSLE). Transcriptomic analysis of FACS sorted primary CD4+ and CD8+ T-cells was performed to assess differential gene expression in patient groups.
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.
