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3D brain vascular niche model captures invasive behavior and gene signatures of glioblastoma

ABSTRACT: 3D brain vascular niche model captures invasive behavior and gene signatures of glioblastoma

PROVIDER: PRJNA1126723 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29494000.fastq.gz	Fastqsanger.gz
	SRR29494001.fastq.gz	Fastqsanger.gz
	SRR29494002.fastq.gz	Fastqsanger.gz
	SRR29494003.fastq.gz	Fastqsanger.gz
	SRR29494004.fastq.gz	Fastqsanger.gz

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3D brain vascular niche model captures invasive behavior and gene signatures of glioblastoma

Project description:Glioblastoma (GBM) is a highly lethal brain cancer with no effective treatments; understanding how GBM cells respond to tumor microenvironment remain challenging as conventional cell cultures lack cytoarchitecture while in vivo models present complexity all at once. Developing a culture system to bridge the gap is thus crucial. Here, we employed a multicellular approach using human glia and vascular cells to optimize a 3-dimensional (3D) brain vascular niche model that enabled not only long-term culture of patient derived GBM cells but also recapitulation of key features of GBM heterogeneity and gene reprogramming in accordance with invasion behaviors and vascular association. Remarkably, vascular contact of GBM cells induced genes concerning neuronal, synaptic, and glia interaction, as well as immune suppression. This gene signature also displayed regional enrichment particularly in leading edge and microvascular proliferation zones and predicted worse prognosis for GBM patients. Furthermore, gene variance analysis uncovered histone demethylation and xylosyltransfererase activity as the main themes for the top induced genes in vivo, signifying the importance of chromatin remodeling and posttranslational modification proteoglygan such as CSPG in GBM adaption. Finally, our model also demonstrated a capacity to maintain GBM quiescence state and a protective niche against chemotherapy. In summary, our 3D model recapitulated key features of GBM heterogeneity and unveiled a previously unappreciated influence of brain glia-vascular unit for transcriptional adaption for neural/synaptic interaction and immunosuppression. The brain vascular niche model may serve as an effective bridge between 2D cultures and in vivo models for GBM modeling and therapeutic development.

2024-07-18 | GSE270481 | GEO

Cardiovascular disease perturbs the vascular hematopoietic stem cell niche

Project description:Hematopoiesis advances cardiovascular disease by generating inflammatory leukocytes that attack the arteries, heart and brain. While it is well documented that the bone marrow niche regulates hematopoietic stem cell proliferation and hence the systemic leukocyte pool, it is less clear how cardiovascular disease affects the vasculature forming this niche. Here we show that arterial hypertension, atherosclerosis and myocardial infarction alter the anatomy and function of bone marrow vasculature. Hypertension and atherosclerosis instigated vascular fibrosis, leakage and endothelial dysfunction in the bone marrow. Myocardial infarction induced vascular leakage and bone marrow angiogenesis via Vegf signaling. Endothelial cell-specific deletion of the Vegf receptor 2 limited emergency hematopoiesis after myocardial infarction, indicating that new vasculature supports higher blood cell production. RNA-sequencing of bone marrow endothelial cells revealed inflammatory gene expression in mice with cardiovascular disease. Endothelial cell-specific deletion of interleukin 6 or versican, which were highly expressed in mice with atherosclerosis or myocardial infarction, respectively, reduced hematopoiesis and systemic myeloid cells. Taken together, cardiovascular disease affects the vascular bone marrow niche, thus influencing hematopoietic stem cell behavior and expanding innate immune cell supply to atherosclerotic plaque and ischemic myocardium. Interrupting this feed back loop may constrain cardiovascular inflammation.

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Mapping the cardiac vascular niche in heart failure

Project description:Mapping the cardiac vascular niche in heart failure

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Vascular niche induction of hematopoietic progenitors from pluripotent stem cells

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 Â± 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 Â± 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

2015-12-31 | E-GEOD-64644 | biostudies-arrayexpress

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Project description:To analyze the role of endothelial derived VEGF-C in the adult bone marrow vascular niche

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