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The DEL-1–β3 integrin axis promotes Runx-1–dependent Foxp3 expression and regulatory T cell responses at mucosal barrier sites

ABSTRACT: The DEL-1–β3 integrin axis promotes Runx-1–dependent Foxp3 expression and regulatory T cell responses at mucosal barrier sites

PROVIDER: PRJNA543235 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9068483.fastq.gz	Fastqsanger.gz
	SRR9068484.fastq.gz	Fastqsanger.gz
	SRR9068485.fastq.gz	Fastqsanger.gz
	SRR9068486.fastq.gz	Fastqsanger.gz
	SRR9068487.fastq.gz	Fastqsanger.gz

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The DEL-1–β3 integrin axis promotes Runx-1–dependent Foxp3 expression and regulatory T cell responses at mucosal barrier sites

Project description:Foxp3+CD4+ regulatory T cells (Tregs) are critical for immune homeostasis and respond to local tissue cues, which control their stability and function. We explored here whether DEL-1, which, like Tregs, increases during resolution of inflammation, promotes Treg responses. DEL-1 enhanced Treg numbers and function at barrier sites (oral and lung mucosa). The underlying mechanism was dissected using mice lacking DEL-1 or expressing a point mutant thereof, or mice with CD4-specific deletion of the transcription factor Runx1, identified by RNA-seq analysis of the DEL-1-induced Treg transcriptome. Specifically, through interaction with avβ3-integrin, DEL-1 promoted induction of Runx1-dependent Foxp3 expression and conferred stability of Foxp3 expression upon Treg restimulation in the absence of exogenous TGFβ1. Additionally, DEL-1 increased RUNX1 and FOXP3 expression in human conventional T cells promoting their conversion into induced Tregs with increased TSDR demethylation, increased stability and suppressive activity. We thus uncovered a DEL-1-avβ3-Runx1 axis that promotes Treg responses at barrier sites and offers novel therapeutic options for modulating inflammatory/autoimmune disorders.

2020-12-31 | GSE131315 | GEO

RNAseq analysis of integrin β3-mediated responses to in vitro docetaxel in PyMT-BO1 breast cancer cells

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Cancer burden is controlled by mural cell- β3-integrin regulated crosstalk with tumor cells

Project description:Phosphoproteomics analysis were performed in WT and β3-integrin-null pericytes. On the other hand, phosphoproteomics experiments were done in B16F0 melanoma cells treated for 24 hours with conditioned medium from WT and β3-integrin-null pericytes.

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RNAseq analysis of integrin β3-mediated responses to in vitro docetaxel in 4T1 breast cancer cells

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The Itgb3 Adhesome - Integrin β3 is seen as a key anti-angiogenic target for cancer treatment due to its expression on neovasculature

Project description:Integrin β3 is seen as a key anti-angiogenic target for cancer treatment due to its expression on neovasculature, but the role it plays in the process is complex; whether it is pro- or anti-angiogenic depends on the context in which it is expressed. To understand precisely β3’s role in regulating integrin adhesion complexes in endothelial cells, we characterised, by mass spectrometry, the β3-dependent adhesome. We show that depletion of β3-integrin in this cell type leads to changes in microtubule behaviour that control their migration. β3-integrin regulates microtubule stability in endothelial cells through Rcc2/Anxa2 driven control of active Rac1 localisation. Our findings reveal that angiogenic processes, both in vitro and in vivo, are more sensitive to microtubule targeting agents when β3-integrin levels are reduced.

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IGDQ motogenic peptide gradient induces directional cell migration through integrin (αv)β3 activation in metastatic breast cancer

Project description:In the context of breast cancer metastasis study, we have shown in an in vitro model of cell migration that IGDQ-exposing (IsoLeu-Gly-Asp-Glutamine type I Fibronectin motif) monolayers (SAMs) on gold sustain the adhesion of MDA-MB-231 cells by triggering Focal Adhesion Kinase by activating integrins. Such tunable scaffolds are used to mimic the extracellular environment, inducing and controlling cell migration towards an anisotropic surface. The observed migratory behavior induced by the IGDQ-bearing peptide gradient along the surface suggests the presence of cell subpopulations: “stationary” or a “migratory” phenotype. We focused on the integrins α5(β1) and (αv)β3, already known to be implicated in cell migration. To this aim, a whole proteomic analysis was performed in beta 3 integrin (ITGB3) or alpha 5 integrin (ITGA5) knock-down MDA-MB-231, in order to highlight the pathways implied into the integrin-dependent cell migration. Our results showed that i) ITGB3 depletion influenced ITGA5 mRNA expression, ii) ITGB3 and ITGA5 were both necessary for IGDQ-mediated directional single cell migration, iii) integrin (αv)β3 was activated by IGDQ fibronectin type I motif and iv) co-regulation of retrograde transport of ITGB3 by ITGA5 is potentially necessary for directional IGDQ-mediated cell migration.

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Project description:Crohn’s disease is a chronic, debilitating inflammatory bowel disease. Here we report a critical role for phospholipase C-β3 (PLC-β3) in intestinal homeostasis. In PLC-β3- deficient mice, exposure to oral dextran sodium sulfate induced lethality and severe inflammation in the small intestine. The lethality was due to PLC-β3 deficiency in multiple non-hematopoietic cell types. PLC-β3 deficiency resulted in reduced Wnt/β-catenin signaling, which is essential for homeostasis and regeneration of the intestinal epithelium. PLC-β3 regulated the Wnt/β-catenin pathway in small intestinal epithelial cells (IECs) at transcriptional, epigenetic, and potentially protein-protein interaction levels. PLC-β3- deficient IECs were unable to respond to stimulation by R-spondin 1, an enhancer of Wnt/β-catenin signaling. Reduced expression of PLC-β3 and its signature genes was found in biopsies of ileal Crohn’s disease patients. PLC-β regulation of Wnt signaling was evolutionally conserved in Drosophila. Our data indicate that reduction of PLC-β3- mediated Wnt/β-catenin signaling contributes to the pathogenesis of ileal Crohn’s disease.

2024-10-06 | GSE244937 | GEO

Integrin beta 3 regulates cellular senescence by activating the TGFβ pathway

Project description:Cellular senescence is an important in vivo mechanism that prevents the propagation of damaged cells. However, the precise mechanism(s) regulating senescence are not well characterized. Here, we find that ITGB3 (integrin beta 3 or β3) is epigenetically regulated by the Polycomb protein CBX7. β3 expression accelerates the onset of senescence in human primary fibroblasts, by activating the TGFβ pathway in a cell autonomous and non-cell autonomous manner. β3 levels are dynamically increased during oncogeneinduced senescence (OIS) through CBX7 epigenetic regulation. DNA-damage and therapy-induced senescence (TIS) also induce β3 expression. In fact, downregulation of β3 levels override OIS and TIS, independently of its ligand-binding activity. Moreover, cilengitide, a αvβ3 antagonist, has the ability to block the SASP without affecting proliferation. Finally, we show an increase in β3 levels during aging in mice and humans. Altogether, our data show that integrin β3 subunit is a marker and regulator of senescence.

2017-03-09 | PXD005717 | Pride

Ileal Crohn’s disease exhibits reduced activity of phospholipase C-β3 (PLC-β3)-dependent Wnt/b-catenin signaling pathway [16S rRNA]

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