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Wnt/β-catenin signaling regulates VE-cadherin-mediated anastomosis of brain capillaries by counteracting S1pr1 signaling

ABSTRACT: Wnt/β-catenin signaling regulates VE-cadherin-mediated anastomosis of brain capillaries by counteracting S1pr1 signaling

PROVIDER: PRJNA495391 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7989640.fastq.gz	Fastqsanger.gz
	SRR7989641.fastq.gz	Fastqsanger.gz
	SRR7989636.fastq.gz	Fastqsanger.gz
	SRR7989637.fastq.gz	Fastqsanger.gz
	SRR7989638.fastq.gz	Fastqsanger.gz

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Similar Datasets

Wnt/β-catenin signaling regulates VE-cadherin-mediated anastomosis of brain capillaries by counteracting S1pr1 signaling

Project description:Canonical Wnt signaling is crucial for vascularization of the central nervous system and blood-brain barrier (BBB) formation. BBB formation and modulation are not only important for development, but also relevant for vascular and neurodegenerative diseases. However, beyond the early requirement of Wnt signaling for brain capillary development, there is little understanding of how Wnt signaling further contributes to brain angiogenesis and BBB formation. By combining high resolution in vivo imaging with temporally and spatially controlled manipulation of Wnt signaling, we were able to dissect different requirements for Wnt signaling during brain angiogenesis and BBB formation. In the absence of Wnt signaling, premature Sphingosine-1-phosphate receptor (S1pr) signaling leads to a reduction of VE-cadherin and Esama at cell-cell junctions. Wnt signaling most likely suppresses S1pr signaling during angiogenesis to enable the dynamic junction formation during anastomosis, whereas later S1pr signaling regulates BBB maturation and VE-cadherin stabilization. Our data provides a novel link between brain capillary angiogenesis and BBB formation and identifies Wnt signaling as coordinator of the timing and as regulator of anastomosis.

2018-10-12 | GSE121041 | GEO

Wnt/β-catenin signaling regulates VE-cadherin-mediated anastomosis of brain capillaries by counteracting S1pr1 signaling.

Project description:Canonical Wnt signaling is crucial for vascularization of the central nervous system and blood-brain barrier (BBB) formation. BBB formation and modulation are not only important for development, but also relevant for vascular and neurodegenerative diseases. However, there is little understanding of how Wnt signaling contributes to brain angiogenesis and BBB formation. Here we show, using high resolution in vivo imaging and temporal and spatial manipulation of Wnt signaling, different requirements for Wnt signaling during brain angiogenesis and BBB formation. In the absence of Wnt signaling, premature Sphingosine-1-phosphate receptor (S1pr) signaling reduces VE-cadherin and Esama at cell-cell junctions. We suggest that Wnt signaling suppresses S1pr signaling during angiogenesis to enable the dynamic junction formation during anastomosis, whereas later S1pr signaling regulates BBB maturation and VE-cadherin stabilization. Our data provides a link between brain angiogenesis and BBB formation and identifies Wnt signaling as coordinator of the timing and as regulator of anastomosis.

| S-EPMC6242933 | biostudies-literature

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

Gene expression profiles of peritoneal macrophages from Sphingosine 1-phosphate receptor type 1 (S1pr1) overexpressing mice against control mice.

Project description:Sphingosine 1-phosphate (S1P) is a lysosphingolipid with anti-atherogenic properties, but mechanisms underlying its effects remain unclear. We here analyzed the consequences of overexpressing the S1P receptor type 1 (S1pr1) on peritoneal macrophage gene expression. To amplify S1pr1 signaling in macrophages, double transgenic mice expressing mouse S1pr1 in mononuclear cells were constructed by crossing two lines. The S1pr1-KI line carries a transgenic cassette in the Rosa 26 locus harboring the mouse S1P1 cDNA and separated from the CAG promoter by a lox-Stop-lox insert. S1pr1-KI mice were then crossed to LysMCre mice expressing Cre recombinase under the control of the lysozyme M promoter, which drives macrophage expression. In the offspring the lox-Stop-lox insert is excised in Cre-expressing cells (macrophages), which induces cDNA expression driven by the CAG promoter. At 12 weeks of age, peritoneal leukocytes were isolated from S1pr1-LysMCre mice and control mice (S1pr1-KI) by peritoneal lavage and seeded in cell culture plates. After 2 h non-adherent cells were removed, total RNA was isolated from the remaining macrophages and subjected to microarray gene expression analysis.

2024-11-07 | E-MTAB-14469 | biostudies-arrayexpress

Cardiomyocyte S1pr1 regulates cardiac regeneration via AKT/mTOR signaling pathway

Project description:Cardiomyocyte S1pr1 regulates cardiac regeneration via AKT/mTOR signaling pathway

| PRJNA1009408 | ENA

S1PR1 Overexpression cells activates endogenous complement signaling and inflammasome to induce tumor metastasis in mice

Project description:Cancer metastasis remains one of the major causes of cancer deaths. The molecular mechanisms of pro-survival lipid signaling activation in inducing cancer cell migration and metastasis are largely unknown. Here, our RNA seq data showed that S1PR1 overexpression B16 melanoma cells injected in C57BL/6 mice via tail vein, activates endogenous complement signaling and inflammasome to induce tumor lung metastasis.

2022-04-15 | GSE172156 | 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

Sphingosine-1 phosphate receptor 1 (S1PR1) is crucial for maintaining the stem cell properties of acute myeloid leukemia stem cells

Project description:To identify the most important gene(s) for maintaining the stem cell properties of leukemia stem cells (LSCs), we analyzed the transcriptional profiles of LSC and non-LSC subsets from acute leukemia patients and identified S1PR1 as a novel biomarker of LSCs. Then to understand the underlying mechanisms of S1PR1-dependent stemness maintenance, we performed gene expression profiling analyses comparing CD34+S1PR1+ and CD34+S1PR1- cell fractions from AML patients and healthy donors; we also determined the global transcriptional response of KG1 cells to an inhibitor of S1PR1 (FTY720) at two concentrations.

2024-08-09 | GSE230423 | GEO

S1PR1 Overexpression cells activates endogenous complement signaling and inflammasome to induce tumor metastasis in mice

Project description:S1PR1 Overexpression cells activates endogenous complement signaling and inflammasome to induce tumor metastasis in mice

| PRJNA722247 | ENA

Cell intrinsic changes in transcription of naïve CD4 T cells upon S1pr1 deletion

Project description:Naïve CD4 cells (CD45.2+CD4+,CD62L high,CD44 low) isolated from lymph nodes of mixed bone marrow chimeras 5 days after induced S1pr1 deletion.

2017-05-26 | GSE97249 | GEO

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