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Immunoglobulins G from Systemic Sclerosis Patients Modify the Molecular Signatures of Endothelial Cells

ABSTRACT: Systemic sclerosis (SSc) is a heterogeneous connective tissue disease characterized by autoimmunity, vasculopathy and excessive fibrosis. Antinuclear antibodies (ANA) are strong diagnostic and prognosis biomarkers but their pathogenicity in fibrosis and vasculopathy remains unclear. Functional antibodies (FA) have been described and might be implicated in the vasculopathy of SSc, in which endothelial cells (EC) are key players. We aimed to explore the effect of purified IgG from SSc patients on omics signature of EC and examine the influence of ANA serotypes or FA.

INSTRUMENT(S): Q Exactive Plus

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Endocardial Cell

DISEASE(S): Systemic Scleroderma

SUBMITTER: BRAY FABRICE

LAB HEAD: fabrice bray

PROVIDER: PXD057210 | Pride | 2025-03-24

REPOSITORIES: Pride

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Immunoglobulins G from Systemic Sclerosis Patients Modify the Proteome of Endothelial Cells Depending on Antinuclear Antibodies Serotypes

Project description:Systemic sclerosis (SSc) is a heterogeneous connective tissue disease characterized by autoimmunity, vasculopathy and excessive fibrosis (1). Antinuclear antibodies (ANA) are strong diagnostic and prognosis biomarkers but their pathogenicity in fibrosis and vasculopathy remains unclear. Functional antibodies (FA) such as angiotensin II type 1 receptor [AT1R] and endothelin-1 type A receptor [ETAR] have been described in SSc and might be implicated in vasculopathy, in which endothelial cells (EC) are key players.We aimed to explore the effect of purified IgG from SSc patients on the proteome of EC and examine the influence of ANA serotypes or FA. The detailed methodology is available in the Supplementary Material section.

2025-03-24 | PXD049364 | Pride

IgG from systemic sclerosis patients induce a profibrosing and serotype-dependent phenotype in normal dermal fibroblast: a multi-omics study

Project description:Autoantibodies (Aab) are frequent in systemic sclerosis (SSc). While recognized as potent biomarkers, their pathogenic role is much debated. This study explored the effect of purified IgG from SSc patients on the phenotype and function of healthy dermal fibroblast (FB) using an innovative multi-omics approach.

2022-06-29 | PXD025885 | Pride

Endothelial response to type I interferon contributes to vasculopathy and fibrosis and predicts disease progression of systemic sclerosis

Project description:Type I interferon (IFN-1) signatures are a hallmark of patients with systemic sclerosis (SSc). However, its significance in clinical stratification and contribution to deterioration still need to be better understood. For hypothesis generation, we performed single-cell RNA sequencing (scRNAseq) on skin biopsies (SSc=4, control =2) using the BD Rhapsody platform. The IFN-1 signature was mapped, functionally investigated in a bleomycin plus IFNα2-adeno-associated virus (IFNA2-AAV) induced model, and verified in an SSc cohort (n=61). Endothelial cells (EC) had the most prominent IFN-1 signature among dermal non-immune cells. The EC IFN-1 signature was increased both in SSc vs. controls and in dcSSc vs. lcSSc. IFNA2-AAV deteriorated bleomycin-induced dermal fibrosis, EndoMT, and perivascular fibrosis and caused blood vessel loss with EC apoptosis. Vascular MX1, an IFN-1 response protein, was significantly increased both in total SSc skin vs. healthy controls and in dcSSc vs. lcSSc. Baseline vascular MX1 performed similarly to skin score in predicting disease progression over 6-34 months in total SSc and was superior in the dcSSc subpopulation. To sum up, the EC IFN-1 signature distinguished SSc skin subtypes and disease progression and may contribute to vasculopathy and fibrosis.

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Expression data from ERK1/2 null endothelial cells

Project description:Angiogenesis is a complex process orchestrated by both growth factors and cell adhesion to the extracellular matrix and is initiated by focal degradation of the vascular basement membrane with subsequent migration and proliferation of endothelial cells (EC). The Ras/Raf/MEK/ERK pathway is critical for EC function during angiogensis. Although in vitro studies implicate ERK1 and ERK2 in EC survival, their precise role in EC function in vivo remains poorly defined. Cre/loxP technology was used to inactivate Erk1 and Erk2 in EC during murine development, resulting in embryonic lethality due to a drastic reduction in angiogenesis. The angiogenic defect was linked to diminished EC proliferation and migration, but not to increased cell apoptosis. Expression of key cell cycle regulators was diminished in the double knockout cells. In addition, both Paxillin and Focal Adhesion Kinase were expressed at lower levels and failed to correctly localize to the cell membrane in EC lacking Erk1 and Erk2, leading to defects in the organization of the cytoskeleton and in cell motility. The results demonstrate that ERK1 and ERK2 coordinate cell proliferation and migration during angiogenesis. Lentivirus infected cells to generate ERK1/2 WT and ERK1/2 DKO endothelial cells were cultured, RNA was extracted and Affymetrix gene expression arrays were performed.

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2021-09-20 | E-MTAB-10936 | biostudies-arrayexpress

Endothelial Cell CD36 Regulates Membrane Ceramide Formation, Exosome Fatty Acid Delivery to Tissues and Circulating Fatty Acid Levels

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2023-07-02 | GSE235988 | GEO

Regulation of host weight gain and lipid metabolism by bacterial bile acid modification in the gut

Project description:Alterations in the gastrointestinal microbiota have been implicated in obesity in mice and humans, but the conserved microbial functions that influence host energy metabolism and adiposity have not been determined. Here we show that bacterial bile salt hydrolase (BSH) controls a microbe-host dialogue which functionally regulates host lipid metabolism and weight gain. Expression of cloned BSH enzymes in the GI tract of gnotobiotic or conventional mice significantly altered plasma bile acid signatures and regulated transcription of key genes involved in lipid metabolism (PPARgamma angptl4), cholesterol metabolism (abcg5/8), gastrointestinal homeostasis (regIIIgamma) and circadian rhythm (dbp, per1/2) in the liver or small intestine. High-level expression of BSH in conventionally raised mice resulted in significant reduction of host weight-gain, plasma cholesterol and liver triglycerides. We demonstrate that bacterial BSH activity significantly impacts systemic metabolic processes and adiposity in the host, and represents a key mechanistic target for the control of obesity and hypercholesterolaemia. Germ free Swiss Webster mice were monocolonised with EC containing the bacterial gene, Bile salt hydroalse. The treatment groups and relevant controls were; 1. Germ Free(GF) n=4 , 2. GF and EC n=4, 3. GF and EC +BSH1 n=4, 4. GF and EC+ BSH2 n=4, 5. GF re-conventionalised (CONV-D) n= 5. The Ileum and Liver were removed and the RNA extracted (RNAeasy plus universal kit (Qiagen), quantified and Microarrays were carried out using mouse Exon ST1.0 arrays (Affymetrix) by Almac Group, Craigavon, Northern Ireland. Analysis and pathway mapping was carried out by ALMAC and using Subio Platform software (Subio Inc) and Genesis Software.

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E. coli rnpb mutants: wild type proxy strain DW2/pFLP-Ec vs. DW2/pFLP-Bs strain

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Project description:Exon-level transcriptome analysis of embryonal carcinoma (EC) and embryonic stem (ES) cell lines. To circumvent difficulties of isolating pure populations of cancer stem cells for the purpose of identifying malignancy-specific gene expression, we have compared exon-resolution transcriptomic profiles of five embryonal carcinoma (EC) cell lines, a histological subtype of germ cell tumour, to their non-malignant caricature, specifically six human embryonic stem (ES) cell lines. Both cell types are readily accessible, and were purified for undifferentiated cells only. We identified a set of 28 differentially expressed genes, many of which had cancer and stemness roles. Overexpression of the recently discovered pluripotency gene NR5A2 in malignant EC cells revealed an intriguing indication of how WNT-mediated dysregulation of pluripotency is involved with malignancy. At the exon-level, alternative splicing events were detected in ZNF195, DNMT3B and PMF1, and alternative promoters were detected for ASH2L and ETV5. These events were validated by RT-PCR-based methods in EC and ES lines, and further explored within a series of 25 primary tumours, where the alternative splicing event in the de novo DNA methyltransferase DNMT3B may have functional consequences. In conclusion, we have identified malignancy-specific gene expression differences within a rigorous pluripotent stem cell context. These findings are of particular interest for both germ cell tumour and ES cell biology, and in general to the concept of cancer stem cells. 5 EC and 6 ES cell lines gown on plastic and feeders respectively were sorted for the pluripotency marker SSEA3, then profiled on the Affymetrix Human Exon 1.0 ST platform. 3 additional EC lines grown on feeders and ES medium were also profiled in the same way. Data was analyzed using Qlucore (PCA), XRAY and limma (gene- and exon-level expression differences) and SAM (two-class pair-wise Significance of Microarrays).

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