Neutrophils stimulation with AVP promote IL36G release
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE249379 | GEO | 2024/12/01
REPOSITORIES: GEO
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Project description:Neutrophils stimulation with AVP promote IL36G release
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Project description:AVP promotes bone marrow myelopoiesis in depression
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Project description:We aimed to characterize transcriptome heterogeneity of human neutrophil at steady state and in response to stress-induced myelopoiesis. We performed single-cell (sc)RNA-Seq on CD15+ neutrophils isolated from isolated from peripheral blood (PB) or bone marrow (BM) samples of healthy controls (PB n=2, BM n=2), G-CSF-treated donors (n=4), patients undergoing hematopoietic stem cell transplantation (HSC-T; n=3) and patients with locally advanced or metastatic pancreatic ductal adenocarcinoma (PDAC; n=5). Moreover, in order to characterize stage specific neutrophil response to type I or type II interferon (IFN), we stimulated ex vivo cord blood (n=3) derived neutrophils with IFN-beta or IFN-gamma and we processed samples for scRNA-Seq.
2022-11-15 | E-MTAB-11188 | biostudies-arrayexpress
Project description:We aimed to characterize transcriptome plasticity of human myeloid cells in response to stress induced myelopoiesis. We performed bulk RNA sequencing (RNA-Seq) analyses of normal density neutrophils (NDNs), low density neutrophils (LDNs), and monocytes isolated from the peripheral blood (PB) of healthy controls (n=19), of G-CSF-treated donors (n=17) as well as of patients receiving hematopoietic stem cell transplantation (HSC-T; n=8), patients with locally advanced or metastatic pancreatic ductal adenocarcinoma (PDAC; n=15) or intraductal papillary mucinous neoplasms (IPMN; n=14). We also analyzed neutrophil differentiation intermediates from bone marrow samples of controls (n=3) or HSC-T patients (n=7). We generated a total of 210 RNA-Seq samples from 73 individuals.
2022-11-29 | E-MTAB-11190 | biostudies-arrayexpress
Project description:Murine bone marrow myeloid progenitors were submitted to SCRNAseq in order to investigate myelopoiesis
2024-05-21 | GSE229208 | GEO
Project description:Bone marrow endothelial cells regulate myelopoiesis in diabetes
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Project description:Neutrophil homeostasis is maintained, in part, by the regulated release of neutrophils from the bone marrow. Constitutive expression of the chemokine CXCL12 by bone marrow stromal cells provides a key retention signal for neutrophils in the bone marrow through activation of its receptor CXCR4. Herein, we show that the ELR chemokines CXCL1 and CXCL2 are constitutively expressed by bone marrow endothelial cells and osteoblasts, and CXCL2 expression is induced in endothelial cells during granulocyte colony-stimulating factor (G-CSF)-induced neutrophil mobilization. Neutrophils lacking CXCR2, the receptor for CXCL1 and CXCL2, are preferentially retained in the bone marrow, reproducing a myelokathexis phenotype. Transient disruption of CXCR4 failed to mobilize CXCR2 neutrophils. However, doubly deficient neutrophils (CXCR2-/- CXCR4-/-) displayed constitutive mobilization, showing that CXCR4 plays a dominant role. Collectively, these data suggest that CXCR2 signaling is a second chemokine axis that interacts antagonistically with CXCR4 to regulate neutrophil release from the bone marrow. We used gene expression microarrays to determine the changes in osteoblasts and bone marrow endothelial cells after G-CSF treatment. 3 untreated and G-CSF-treated osteoblast samples and 4 untreated and G-CSF-treated endothelial samples.
2010-07-14 | E-GEOD-22925 | biostudies-arrayexpress
Project description:Sympathetic nerves have been implicated in the regulation of HSC homeostasis, we investigated whether sympathetic nerves regulated myeloid-biased differentiation of HSCs in CUMS mice. Transcriptome profiling (RNA-seq) and differential gene expression analysis of bone marrow cells were performed. In bone marrow cells of CUMS mice, the expression of arginine vasopressin receptor 2, a receptor of the stress-related neuroendocrine factor AVP, was upregulated through neuroactive ligand-receptor interaction pathway.
2024-12-01 | GSE249380 | GEO
Project description:The paper describes a model of tumor invasion to bone marrow.
Created by COPASI 4.26 (Build 213)
This model is described in the article:
Modeling invasion of metastasizing cancer cells to bone marrow utilizing ecological principles
Kun-Wan Chen, Kenneth J Pienta
Theoretical Biology and Medical Modelling 2011, 8:36
Abstract:
Background: The invasion of a new species into an established ecosystem can be directly compared to the steps involved in cancer metastasis. Cancer must grow in a primary site, extravasate and survive in the circulation to then intravasate into target organ (invasive species survival in transport). Cancer cells often lay dormant at their metastatic site for a long period of time (lag period for invasive species) before proliferating (invasive spread). Proliferation in the new site has an impact on the target organ microenvironment (ecological impact) and eventually the human host (biosphere impact).
Results: Tilman has described mathematical equations for the competition between invasive species in a structured habitat. These equations were adapted to study the invasion of cancer cells into the bone marrow microenvironment as a structured habitat. A large proportion of solid tumor metastases are bone metastases, known to usurp hematopoietic stem cells (HSC) homing pathways to establish footholds in the bone marrow. This required accounting for the fact that this is the natural home of hematopoietic stem cells and that they already occupy this structured space. The adapted Tilman model of invasion dynamics is especially valuable for modeling the lag period or dormancy of cancer cells.
Conclusions: The Tilman equations for modeling the invasion of two species into a defined space have been modified to study the invasion of cancer cells into the bone marrow microenvironment. These modified equations allow a more flexible way to model the space competition between the two cell species. The ability to model initial density, metastatic seeding into the bone marrow and growth once the cells are present, and movement of cells out of the bone marrow niche and apoptosis of cells are all aspects of the adapted equations. These equations are currently being applied to clinical data sets for verification and further refinement of the models.
To cite BioModels Database, please use: BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models .
To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide.
Please refer to CC0 Public Domain Dedication for more information.
2024-09-02 | BIOMD0000000793 | BioModels
Project description:The paper describes a model of tumor invasion to bone marrow.
Created by COPASI 4.26 (Build 213)
This model is described in the article:
Modeling invasion of metastasizing cancer cells to bone marrow utilizing ecological principles
Kun-Wan Chen, Kenneth J Pienta
Theoretical Biology and Medical Modelling 2011, 8:36
Abstract:
Background: The invasion of a new species into an established ecosystem can be directly compared to the steps involved in cancer metastasis. Cancer must grow in a primary site, extravasate and survive in the circulation to then intravasate into target organ (invasive species survival in transport). Cancer cells often lay dormant at their metastatic site for a long period of time (lag period for invasive species) before proliferating (invasive spread). Proliferation in the new site has an impact on the target organ microenvironment (ecological impact) and eventually the human host (biosphere impact).
Results: Tilman has described mathematical equations for the competition between invasive species in a structured habitat. These equations were adapted to study the invasion of cancer cells into the bone marrow microenvironment as a structured habitat. A large proportion of solid tumor metastases are bone metastases, known to usurp hematopoietic stem cells (HSC) homing pathways to establish footholds in the bone marrow. This required accounting for the fact that this is the natural home of hematopoietic stem cells and that they already occupy this structured space. The adapted Tilman model of invasion dynamics is especially valuable for modeling the lag period or dormancy of cancer cells.
Conclusions: The Tilman equations for modeling the invasion of two species into a defined space have been modified to study the invasion of cancer cells into the bone marrow microenvironment. These modified equations allow a more flexible way to model the space competition between the two cell species. The ability to model initial density, metastatic seeding into the bone marrow and growth once the cells are present, and movement of cells out of the bone marrow niche and apoptosis of cells are all aspects of the adapted equations. These equations are currently being applied to clinical data sets for verification and further refinement of the models.
To cite BioModels Database, please use: BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models .
To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide.
Please refer to CC0 Public Domain Dedication for more information.
2024-09-02 | BIOMD0000000795 | BioModels