VISTA is an activating receptor that binds the proteoglycan Syndecan-2 on monocytes.
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA726958 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR14407440.fastq.gz | Fastqsanger.gz | |||
| SRR14407441.fastq.gz | Fastqsanger.gz | |||
| SRR14407442.fastq.gz | Fastqsanger.gz | |||
| SRR14407443.fastq.gz | Fastqsanger.gz | |||
| SRR14407444.fastq.gz | Fastqsanger.gz |
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Project description:As indicated by its name, V-domain Ig suppressor of T cell activation (VISTA) is thought to primarily serve as an inhibitory protein that limits immune responses. VISTA-antibodies can dampen the effects of several concomitantly elicited activation signals including T cell receptor (TCR) and Toll-like receptor (TLR) activation, but it is currently unclear if VISTA agonism could singly affect immune cell biology. In this study, we discovered two novel agonistic VISTA antibodies and characterized their effects on human peripheral blood mononuclear cells (PBMC) by scRNA/CITE-seq. Both antibodies agonize VISTA in an Fc-functional manner to elicit transcriptional and functional changes in monocytes consistent with activation. We also used pentameric VISTA to identify Syndecan-2 (Sdc2) and several heparan sulfate proteoglycan (HSPG) synthesis genes as novel regulators of VISTA binding to monocytic cells adding further evidence of bidirectional signaling. Together, our study highlights several novel aspects of VISTA biology that have yet to be uncovered in myeloid cells and serves as a foundation for future research.
2021-05-04 | GSE173747 | GEO
Project description:Syndecan-2 was found to act as a tumor suppressor in osteosarcoma and to mediate the apoptotic response to cytotoxic agents. To determine new mechanisms that control cell survival and apoptosis in osteosarcoma cells, we aim to show target genes that are involved downstream of this proteoglycan during apoptosis induction. We aim to compare the modifications induced by syndecan-2 overexpression in two different human osteosarcoma cell lines using a lentiviral vector coding the human syndecan-2. Syndecan-2 lentiviral vector (SY) and control empty lentiviral vector (VV) were transducted in two different human osteosarcoma cell lines in a dye-swap experiment.
2013-09-23 | E-GEOD-19913 | biostudies-arrayexpress
Project description:Syndecan-2 was found to act as a tumor suppressor in osteosarcoma and to mediate the apoptotic response to cytotoxic agents. To determine new mechanisms that control cell survival and apoptosis in osteosarcoma cells, we aim to show target genes that are involved downstream of this proteoglycan during apoptosis induction. We aim to compare the modifications induced by syndecan-2 overexpression in two different human osteosarcoma cell lines using a lentiviral vector coding the human syndecan-2.
2013-09-23 | GSE19913 | GEO
Project description:V-domain immunoglobulin suppressor of T-cell activation (VISTA) has emerged as a unique immunoregulatory receptor on cells of the myeloid lineage. Agonizing VISTA on myeloid cells has recently been demonstrated to have a profound effect on dampening inflammatory responses. VISTA has been proposed to function both as a ligand and as a receptor, yet the role of VISTA as a ligand has been largely ignored. In this experiment, macrophages and neutrophils were isolated from mice and treated with LPS and VISTA to examine the effect of VISTA in dampening acute inflammation.
2022-12-02 | E-MTAB-10856 | biostudies-arrayexpress
Project description:Biomechanical stimuli and extracellular matrix cues are important initiators for the cardiac remodeling process, and signaling hubs in the sarcolemma are important contact points between the extracellular space and cell interior, sensing and transducing biomechanical signals into a cellular response. The transmembrane proteoglycan syndecan-4 localizes to these attachment points and has been shown important in initial stages of cardiac remodeling. The objective of this study was to map the cardiac interactome of syndecan-4 to better understand its function and downstream signaling mechanisms. By combining two different affinity purification methods with mass spectrometry, we identified the cardiac syndecan-4 interactome to consist of 21 novel and 31 previously described interaction partners. 12of the novel partners were further validated to bind syndecan-4 in HEK293 (MPP7, PARVB, CCT5, CDK9, EIF22S1, PFKM, RASIP, EIF4B, PTRF/CAVIN1, AP3D1, EPB4.1 and MLP/CSRP3). 19 of the interactome partners bound differently to syndecan-4 in left ventricle lysate from aorta banded hypertrophic failing (ABHF) rats. One of these partners was the well-known mechanotransducer MLP, which showed a direct and significant increased binding to syndecan-4 in ABHF. Nuclear translocation is important in MLP mediated signalling and we found less MLP in nuclear enriched fractions from syndecan-4-/- mouse left ventricles, but an increase in nuclear MLP when syndecan-4 was overexpressed in a cardiomyocyte cell line. In the presence of a cell-permeable syndecan-4-MLP disruptor peptide, the nuclear MLP level was significantly reduced. This suggests syndecan-4 to be a mediator of nuclear translocation of MLP in the heart.
2019-04-09 | PXD011249 | Pride
Project description:1) BMDMs treated with anti-VISTA under tolerizing and immunizing conditions. 2) Time course analysis of anti-VISTA-induced alterations in human monocytes after anti-VISTA treatment. 3) Time course analysis of anti-VISTA-induced alterations in BMDMs after anti-VISTA treatment. 4) Single cell ATAC-seq of BMDMs tolerized in the presence or IgG or anti-VISTA.
2020-09-05 | GSE157518 | GEO
Project description:Backgrounds: The present study addressed whether V-domain Ig suppressor of T cell activation (VISTA), constitutively expressed in kidney macrophages, has a protective role in tubulointerstitial fibrotic transformation after acute antibody-mediated glomerulonephritis. Methods: Wild-type (WT) and VISTA-deficient (Vsir-/-, KO) mice were treated with nephrotoxic serum to induced acute antibody-mediated glomerulonephritis, and their cytokine and fibrosis profiles were compared. Results: VISTA was highly expressed in kidney macrophages (resident more than infiltrating subset). If VISTA was depleted, tubules suffered further damage after glomerular injury. In damaged Vsir–/– mice, the contact frequency of macrophages with infiltrated T cells increased, and then the immunometabolic characteristics of T cells changed to overproduction of interferon-γ. The Vsir–/– parenchymal tissue cells responded to this altered milieu as more producing interleukin-9, which augmented tubulointerstitial fibrosis and irreversible kidney dysfunction. The blocking antibodies against interferon-γ and interleukin-9 protected above pathological process by VISTA depletion. Conclusions: VISTA is a sentinel protein of kidney macrophages, which prevents tubulointerstitial fibrosis via interferon-γ-interleukin-9 axis after acute antibody-mediated glomerular injury.
2021-08-04 | GSE181163 | GEO
Project description:Analysis of how Syndecan-2 expression identifies hematopoietic stem cells with unique gene expression profiles. We tested the hypothesis that Syndecan-2 expression enriches for hematopoietic stem cell gene expression programs. The results provide important insight into how Syndecan-2 can be used to isolate hematopoietic stem cells with distinct hematopoietic properties.
2022-03-09 | GSE151733 | GEO
Project description:We evaluated the effect of syndecan-1 in various cell-based and animal models of lung cancer and found that lung tumorigenesis was promoted when cells lose syndecan-1 expression. We also demonstrate that syndecan-1 (or lack thereof) alters the microRNA (miRNA) cargo carried within exosomes exported from lung cancer cells. Analysis of the changes in miRNA expression identifies a distinct shift toward augmented pro-cancerous signaling, which are consistent with the changes found in lung adenocarcinoma. In all, our work identifies syndecan-1 as an important factor on lung cancer cells that control its ability to shape the lung tumor microenvironment through alterations in miRNA packaging within exosomes.
2017-10-30 | GSE106303 | GEO
Project description:We evaluated the effect of syndecan-1 in various cell-based and animal models of lung cancer and found that lung tumorigenesis was promoted when cells lose syndecan-1 expression. We also demonstrate that syndecan-1 (or lack thereof) alters the microRNA (miRNA) cargo carried within exosomes exported from lung cancer cells. Analysis of the changes in miRNA expression identifies a distinct shift toward augmented pro-cancerous signaling, which are consistent with the changes found in lung adenocarcinoma. In all, our work identifies syndecan-1 as an important factor on lung cancer cells that control its ability to shape the lung tumor microenvironment through alterations in miRNA packaging within exosomes.
2017-10-28 | GSE106277 | GEO