Danio rerio
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA358009 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5119923_1.fastq.gz | Fastqsanger.gz | |||
| SRR5119923_2.fastq.gz | Fastqsanger.gz | |||
| SRR5119924_1.fastq.gz | Fastqsanger.gz | |||
| SRR5119924_2.fastq.gz | Fastqsanger.gz | |||
| SRR5119925_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 8 |
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Project description:CXCL8 and CXCR1 Remodel the Vascular Niche to Promote Hematopoietic Stem and Progenitor Cell Colonization and Engraftment
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Project description:CXCL8 and CXCR1 Remodel the Vascular Niche to Promote Hematopoietic Stem and Progenitor Cell Colonization and Engraftment [huvec CXCL8 vs control]
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Project description:The microenvironment is an important regulator of hematopoietic stem and progenitor cell (HSPC) biology. Interactions between the niche and stem cells have been difficult to track, but recent advances marking fluorescent HSPCs have allowed exquisite visualization in the caudal hematopoietic tissue (CHT) of the developing zebrafish. Sinusoidal endothelial cells interact closely with HSPCs as they colonize this niche. Here we show that the chemokine cxcl8 and its receptor, cxcr1, are abundantly expressed by zebrafish endothelial cells and we identify cxcl8/cxcr1 signaling as a positive regulator of HSPC colonization using genetic gain- and loss-of-function techniques. Single-cell tracking experiments demonstrated that this effect is due to an increase in HSPC “cuddling” by endothelial cells, thereby increasing CHT residency time and allowing more HSPC cell divisions to occur. Enhanced cxcl8/cxcr1 signaling was associated with an increase in the volume of the CHT and induction of cxcl12a expression, favoring HSPC colonization. Finally, using parabiotic zebrafish, we show that cxcr1 acts stem cell non-autonomously to improve the efficiency of donor HSPC engraftment. This work identifies a mechanism by which the hematopoietic niche remodels to promote HSPC engraftment and suggests that cxcl8/cxcr1 signaling is a potential therapeutic target in patients undergoing hematopoietic stem cell transplantation.
2017-03-24 | GSE92541 | GEO
Project description:The microenvironment is an important regulator of hematopoietic stem and progenitor cell (HSPC) biology. Interactions between the niche and stem cells have been difficult to track, but recent advances marking fluorescent HSPCs have allowed exquisite visualization in the caudal hematopoietic tissue (CHT) of the developing zebrafish. Sinusoidal endothelial cells interact closely with HSPCs as they colonize this niche. Here we show that the chemokine cxcl8 and its receptor, cxcr1, are abundantly expressed by zebrafish endothelial cells and we identify cxcl8/cxcr1 signaling as a positive regulator of HSPC colonization using genetic gain- and loss-of-function techniques. Single-cell tracking experiments demonstrated that this effect is due to an increase in HSPC “cuddling” by endothelial cells, thereby increasing CHT residency time and allowing more HSPC cell divisions to occur. Enhanced cxcl8/cxcr1 signaling was associated with an increase in the volume of the CHT and induction of cxcl12a expression, favoring HSPC colonization. Finally, using parabiotic zebrafish, we show that cxcr1 acts stem cell non-autonomously to improve the efficiency of donor HSPC engraftment. This work identifies a mechanism by which the hematopoietic niche remodels to promote HSPC engraftment and suggests that cxcl8/cxcr1 signaling is a potential therapeutic target in patients undergoing hematopoietic stem cell transplantation.
2017-03-24 | GSE92542 | GEO
Project description:CXCL8 is produced by many cell types including epithelial, endothelial, fibroblasts and macrophages in response to TLR recognition of microbe-associated molecular patterns (MAMPs) or inflammatory cytokines and recruits phagocytes from the vasculature to sites of infection via interaction with its cognate receptors CXCR1 and CXCR2. In the intestine, CXCL8 has been demonstrated to participate in the migration of neutrophils across the epithelium during acute inflammation. Given the well-recognized role of CXCL8 as an initiator of inflammation and the constant presence of commensal bacteria in the intestinal tract, we hypothesized that in the intestinal epithelium, CXCL8 might be secreted in a vectorial fashion depending on the location and type of stimulus as a mechanism to maintain homeostasis. In addition, we hypothesized that the CXCR1 receptor might control specific functions in polarized IECs depending on its location. We tested these hypotheses using microarray gene expression profiling of IL-8 treated and mock-treated Caco-2 cell lines This study was set up according to a one-treatment, one-control design. It contains individual transcriptional profiles from 3 IL-8-treated and 3 buffer control-treated samples. In total, this study includes data from 3 Caco-2 samples x 2 treatments=6 arrays.
2014-06-28 | E-GEOD-30364 | biostudies-arrayexpress
Project description:CXCL8 is produced by many cell types including epithelial, endothelial, fibroblasts and macrophages in response to TLR recognition of microbe-associated molecular patterns (MAMPs) or inflammatory cytokines and recruits phagocytes from the vasculature to sites of infection via interaction with its cognate receptors CXCR1 and CXCR2. In the intestine, CXCL8 has been demonstrated to participate in the migration of neutrophils across the epithelium during acute inflammation. Given the well-recognized role of CXCL8 as an initiator of inflammation and the constant presence of commensal bacteria in the intestinal tract, we hypothesized that in the intestinal epithelium, CXCL8 might be secreted in a vectorial fashion depending on the location and type of stimulus as a mechanism to maintain homeostasis. In addition, we hypothesized that the CXCR1 receptor might control specific functions in polarized IECs depending on its location. We tested these hypotheses using microarray gene expression profiling of IL-8 treated and mock-treated Caco-2 cell lines
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Project description:Metastasis is the primary cause of cancer-related mortality and the mechanistically least well understood step of the tumor progression cascade. Employing surgical preclinical metastasis models, we show here that small primary tumors reprogram the body’s vascular endothelium to alter systemic homeostasis and to condition the premetastatic niche for metastatic colonization. Endothelial cells thereby serve as an amplifier of tumor-induced instructive signals. The combined endothelial transcriptomic and serum proteomic screen identified the TGFß pathway signaling specifier LRG1 as an early vascular niche instructor of metastatic colonization. Adjuvant LRG1 inhibition to primary tumor-resected mice delayed metastatic growth and increased overall survival. The study has thereby established the premetastatic systems map of primary tumor-induced vascular changes and identified LRG1 as a therapeutic target for metastasis
2022-05-16 | PXD013978 | Pride
Project description:Pluripotent stem cells (PSC) represent an alternative source of hematopoietic stem cells (HSCs). Clinical translation is impeded by limited engraftment of human (h)PSC-multipotent progenitor cells (MPP). This barrier suggests that additional cues are required for definitive hematopoiesis. We hypothesized that vascular niche producing Notch ligands Jagged-1 (JAG1) and Delta-like ligand-4 (DLL4) would drive definitive hematopoiesis. To test our hypothesis, hes2 human embryonic stem cells (hESC) 2 and Macaca nemestrina (Mn) iPSC line-7 were differentiated with cytokines ± endothelial cells (EC), which express JAG1 and DLL4. EC co-culture supported emergence of 8-fold more CD34+CD45+ cells compared to co-culture with cytokines ± ECs with JAG1 or DLL4 knockdown. EC-induced cells exhibit Notch activation and express HSC-specific targets of Notch signaling RUNX1 and GATA2. EC-induced PSC-MPP engraft at a higher level in NSG mice compared to cytokine-induced cells (10% >5 months), and selection increased engraftment (30%). Long-term engraftment and the myeloid-to-lymphoid ratio achieved with vascular niche induction is similar to levels achieved for cord blood MPP and up to 20-fold higher than hPSC-MPP engraftment. Our findings identify a previously underappreciated role for endothelial Notch ligands in PSC definitive hematopoiesis and production of long-term engrafting CD34+ cells and suggest they are critical for HSC emergence. Transcriptome sequencing of Macaca nemestrina (Mn) iPSCs
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