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The age of the bone marrow microenvironment influences B-cell acute lymphoblastic leukemia progression via CXCR5-CXCL13 [RNA-Seq]

ABSTRACT: The age of the bone marrow microenvironment influences B-cell acute lymphoblastic leukemia progression via CXCR5-CXCL13 [RNA-Seq]

PROVIDER: PRJNA753841 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15417448_1.fastq.gz	Fastqsanger.gz
	SRR15417448_2.fastq.gz	Fastqsanger.gz
	SRR15417449_1.fastq.gz	Fastqsanger.gz
	SRR15417449_2.fastq.gz	Fastqsanger.gz
	SRR15417450_1.fastq.gz	Fastqsanger.gz

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The age of the bone marrow microenvironment influences B-cell acute lymphoblastic leukemia progression via CXCR5-CXCL13

Project description:The age of the bone marrow microenvironment influences B-cell acute lymphoblastic leukemia progression via CXCR5-CXCL13

| PRJNA755248 | ENA

The age of the bone marrow microenvironment influences B-cell acute lymphoblastic leukemia progression via CXCR5-CXCL13 [ATAC-Seq]

Project description:The age of the bone marrow microenvironment influences B-cell acute lymphoblastic leukemia progression via CXCR5-CXCL13 [ATAC-Seq]

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The age of the bone marrow microenvironment influences B-cell acute lymphoblastic leukemia progression via CXCR5-CXCL13.

Project description:B-cell acute lymphoblastic leukemia (B-ALL) occurs most commonly in children, whereas chronic myeloid leukemia is more frequent in adults. The myeloid bias of hematopoiesis in elderly individuals has been considered causative, but the age of the bone marrow microenvironment (BMM) may be contributory. Using various murine models of B-ALL in young vs old mice, we recapitulated B-ALL preponderance in children vs adults. We showed differential effects of young vs old BM macrophages on B-ALL cell function. Molecular profiling using RNA- and ATAC-sequencing revealed pronounced differences in young vs old BMM-derived macrophages and enrichment for gene sets associated with inflammation. In concordance with the role of C-X-C motif chemokine (CXCL) 13 for disease-associated B-cell chemoattraction, we found CXCL13 to be highly expressed in young macrophages on a translational compared with a transcriptional level. Inhibition of CXCL13 in BM macrophages impaired leukemia cell migration and decreased the proliferation of cocultured B-ALL cells, whereas recombinant CXCL13 increased pAKT and B-ALL cell expansion. Pretreatment of B-ALL-initiating cells with CXCL13 accelerated B-ALL progression. Deficiency of Cxcr5, the receptor for CXCL13, on B-ALL-initiating cells prolonged murine survival, whereas high expression of CXCR5 in pediatric B-ALL may predict central nervous system relapse. CXCL13 staining was increased in bone sections from pediatric compared with adult patients with B-ALL. Taken together, our study shows that the age of the BMM and, in particular, BM macrophages influence the leukemia phenotype. The CXCR5-CXCL13 axis may act as prognostic marker and an attractive novel target for the treatment of B-ALL.

| S-EPMC8767790 | biostudies-literature

PROTEIN KINASE C EPSILON COOPERATES WITH PTEN LOSS FOR PROSTATE TUMORIGENESIS THROUGH THE CXCL13-CXCR5 PATHWAY

Project description:PKCe, an oncogenic member of the PKC family, is aberrantly overexpressed in epithelial cancers. To date, little is known about functional interactions of PKCe with other genetic alterations and the effectors of this kinase that contribute to its tumorigenic and metastatic phenotype. Here we demonstrate that PKCe cooperates with the loss of the tumor suppressor Pten for the development of prostate cancer in a mouse model. Mechanistic analysis revealed that PKCe overexpression and Pten loss individually and synergically cause a remarkable up-regulation in the production of the chemokine CXCL13. Notably, targeted disruption of CXCL13 or its receptor CXCR5 in prostate cancer cells impaired their migratory and tumorigenic properties. In addition to providing evidence for an autonomous vicious cycle driven by PKCe, our studies identified a compelling rationale for targeting the CXCL13:CXCR5 axis for prostate cancer treatment.

2017-04-01 | GSE86257 | GEO

The age of the bone marrow microenvironment influences B-cell acute lymphoblastic leukemia progression via CXCR5-CXCL13

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-08-24 | GSE182174 | GEO

The healing myocardium mobilizes a distinct B-cell subset through a CXCL13-CXCR5-dependent mechanism

Project description:Recent studies have revealed that B-cells can influence post-myocardial infarction (MI) inflammation and repair, but the mechanisms controlling their mobilization and in situ activity remain poorly understood. Herein, we sought to dissect the mechanisms underlying B-cell cardiotropism and assess the B-cell antigen specificity profile in an experimental model of MI. Our study reveals that B-cells that are not antigen-specifically expanded readily infiltrate the infarcted myocardium via the CXCL13-CXCR5 axis. The restricted distribution of CXCR5 among hB cells could offer a suitable opportunity to selectively target this leukocyte subset therapeutically while minimally interfering with other local or systemic immunological processes.

2021-05-29 | GSE150140 | GEO

The age of the bone marrow microenvironment influences B-cell acute lymphoblastic leukemia progression via CXCR5-CXCL13 [ATAC-Seq]

Project description:We performed ATAC sequencing to determine if epigenetic changes regulate the function of young versus old macrophages.

2021-08-24 | GSE182172 | GEO

The age of the bone marrow microenvironment influences B-cell acute lymphoblastic leukemia progression via CXCR5-CXCL13 [RNA-Seq]

Project description:We performed RNA sequencing to determine the alteration in the molecular landscape in young versus old macrophages.

2021-08-24 | GSE181908 | GEO

Disturbed glycolipid metabolism activates CXCL13-CXCR5 axis in senescent TSCs to promote heterotopic ossification formation

Project description:Heterotopic ossification (HO) occurs as a common complication after injury, while its risk factor and mechanism remain unclear yet, which restricts the development of pharmacological treatment. Clinical research suggested that diabetes mellitus (DM) patients were prone to develop HO in tendon, but the solid evidence and mechanical research are still needed. Here, we combined the clinical samples and DM mice model to identify that disordered glycolipid metabolism aggravates the senescence of tendon derived stem cells (TSCs) and promotes their osteogenic differentiation. Then, combining the RNA-seq results of aging tendon, we detected the abnormally activated autocrine CXCL13-CXCR5 axis in TSCs cultured in high fat high glucose (HFHG) environment and also in aged tendon. Genetic inhibition of CXCL13 successfully alleviates the HO formation in DM mice, providing a potential therapeutical target for suppressing HO formation in DM patients after trauma or surgery.

2024-08-28 | GSE234916 | GEO

Lack of chemokine signaling through CXCR5 causes mortality, ventricular dilatation and deranged matrix during pressure overload

Project description:Inflammatory mechanisms have been suggested to play a role in the development of heart failure (HF), but a role for chemokines is largely unknown. The aim of this study was to analyze the role of the chemokine CXCL13 and its receptor CXCR5 in cardiac pathophysiology leading to HF A microarray study was performed on seven mice harboring a systemic knockout of the CXCR5 (CXCR5-/-) and seven wildtype mice. Four of the knockouts and four of the wild type mice were subjected to aorta banding and three of each to sham operations.

2010-10-01 | E-GEOD-22295 | biostudies-arrayexpress

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