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Marginal zone B cells receive robust Notch2 signals within the B cell follicle in the absense of S1pr1 signaling.

ABSTRACT: Marginal zone B cells receive robust Notch2 signals within the B cell follicle in the absense of S1pr1 signaling.

PROVIDER: PRJNA1148923 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30273500.fastq.gz	Fastqsanger.gz
	SRR30273501.fastq.gz	Fastqsanger.gz
	SRR30273502.fastq.gz	Fastqsanger.gz
	SRR30273503.fastq.gz	Fastqsanger.gz
	SRR30273504.fastq.gz	Fastqsanger.gz

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Marginal zone B cells receive robust Notch2 signals within the B cell follicle in the absense of S1pr1 signaling.

Project description:Marginal zone (MZ) B cells have innate-like response characteristics due to a unique ability receive and integrate Notch2 signals in the spleen. There is evidence showing MZ B cells receive these signals both in the marginal sinus and the B cell follicle. The relative strength and conservation of these Notch signals is not yet clear. Therefore, we generated mice in which S1pr1 is deleted in mature B cells. These mice have MZ B cells by phenotype but these cells are retained in the follicle and unable to transit to the marginal zone. In this experiment we examined the impact of Notch2 signaling in these cells and cre expressing control animals using in vivo anti-Notch2 antibody blockade followed by RNA-sequencing.

2024-10-18 | GSE274990 | GEO

Identification of Myc-dependent and -independent Notch2 signatures in marginal zone B cells.

Project description:Marginal zone (MZ) B cells leverage Notch2 signals to attain rapid differentiation responses and positional cues with in the spenic environment. While it is known that a major player in Notch2 signaling in MZ B cells is the proto-oncogene Myc, it is not clear to what extent MZ B cells use Notch2 signals in Myc-independent manner. In this study we conditinally and inducibly deleted Myc in mature B cells and then used in vivo delivery of anti-Notch2 antibodies to separated Myc-dependent and -independent Notch2 signaling in MZ B cells.

2024-10-18 | GSE274989 | GEO

Transcriptomic analyis follicular and marginal zone B ells after in vivo Notch2 blockade.

Project description:Marginal zone B cells which make rapid mitosis-independent plasma cell responses are dependent on Notch2 signaling for their generation and maintenance. In order to determine the effect of ongoing Notch signaling on the maintenance of the MZ transcriptome, we performed RNA-seq on MZ and follicular B cells after 12, 24 and 48 hours of in vivo Notch2 antibody blockade

2021-07-22 | GSE180172 | GEO

Notch2 Signaling Induces Trans-differentiation of Follicular to Marginal Zone B Cells

Project description:Notch2 Signaling Induces Trans-differentiation of Follicular to Marginal Zone B Cells

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Identification of Myc-dependent and -independent Notch2 signatures in marginal zone B cells.

Project description:Identification of Myc-dependent and -independent Notch2 signatures in marginal zone B cells.

| PRJNA1148917 | ENA

Transcriptomic analyis follicular and marginal zone B ells after in vivo Notch2 blockade.

Project description:Transcriptomic analyis follicular and marginal zone B ells after in vivo Notch2 blockade.

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Human splenic marginal zone precursors (MZP) differentiation into marginal zone B cells (MZB)through a Notch2 signalling pathway

Project description:RNA microarray profiling analysis was performed on different ex-vivo human splenic B cell subsets (M-^SNaM-oveM-^T, marginal zone precursors or M-^SMZPM-^T, marginal zone B cells orM-^T MZBM-^T, M-^SMTG+CD45+M-^T cells) and on M-^Sp27M-^T cells, corresponding to the fraction of MZP cells that differentiated into CD27-expressing cells after culture on OP9-hDLL1 cells cultured with OP9-hDLL1 cells that differentiated into CD27-expressing cells

2014-03-26 | E-MTAB-2244 | biostudies-arrayexpress

NOTCH2 mutants

Project description:NOTCH2 mutants

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Cardiomyocyte S1pr1 regulates cardiac regeneration via AKT/mTOR signaling pathway

Project description:Mammalian hearts had the capability to regenerate cardiomyocyte and completely recover after heart injury within a limited time window after birth. It has been shown that sphingosine 1-phospahte receptor 1 (S1pr1) was highly expressed in cardiomyocytes and played an important role in heart development and pathological cardiac remodeling. Herein, we aim to investigate the role of CM-S1pr1 for cardiac regeneration and tissue repair after heart injury. We generated cardiomyocyte (CM)-specific S1pr1 knock-out mice and showed that CM-specific S1pr1 loss-of-function significantly severely reduced cardiomyocyte proliferation and heart regeneration in neonatal mice after both apex resection and myocardial infarction, whereas S1pr1 gain-of-function by AAV9-mediated CM-specific overexpression of S1pr1 significantly boosted cardiac regeneration and improved cardiac functions after heart injuries. We next identified that S1pr1 activated AKT/mTOR/CyclinD1 and Bcl-2 signaling pathways, and thus promoted cardiomyocyte proliferation and inhibited CM apoptosis, respectively.Of note, we applied CM-targeted gene therapy by AAV9-cTNT to specifically overexpress S1pr1 in cardiomyocytes and achieved an efficient S1pr1 overexpression in CMs in vivo. This CM-targeted strategy to overexpress S1pr1 significantly enhanced cardiac regeneration and improved cardiac functions after myocardial infarction in an adult mouse model, suggesting a potential strategy to boost adult cardiac regeneration in vivo.

2024-08-01 | GSE241722 | GEO

Programming to S1PR1+ Endothelial Cell Promotes Restoration of Lung Vascular Integrity

Project description:Increased endothelial permeability and failure to repair is the hallmark of several vascular diseases including acute lung injury (ALI). However, little is known about the intrinsic pathways that activate endothelial cell (EC) regenerative programs and thereby tissue repair. Studies have invoked a crucial role of sphingosine-1-phosphate (S1P) in resolving endothelial hyperpermeability through activation of the G-protein coupled receptor, sphingosine-1-phosphate receptor 1 (S1PR1). Here, we addressed mechanisms of generation of S1PR1+ EC, which may prevent endothelial injury. Studies were made using inducible EC-S1PR1-/- (iEC-S1PR1-/-) mice and S1PR1-GFP reporter mice to trace the generation of S1PR1+ EC. We observed in a mouse model of endotoxemia that S1P generation induced the programming of S1PR1lo to S1PR1+ EC, which comprised 80% of lung EC. The transition of these cells was required for reestablishing the endothelial barrier. We also observed that conditional deletion of S1PR1 in EC increased vascular permeability. RNA-seq analysis of S1PR1+ EC showed enrichment of genes regulating S1P synthesis and transport, sphingosine kinase 1 (SPHK1) and SPNS2, respectively. The activation of transcription factors EGR1 and STAT3 were essential for transcribing SPHK1 and SPNS2, respectively, to increase S1P production that served to amplify S1PR1+ EC transition. Transplantation of S1PR1+ EC into injured lung vasculature restored endothelial integrity. Our findings show that generation of a S1PR1+ EC population activates the endothelial regenerative program mediating vascular endothelial repair, thus raising the possibility of harnessing this pathway to restore vascular homeostasis in inflammatory injury.

2023-01-15 | GSE165000 | GEO

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