Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Cellular Indexing of Transcriptomes and epitopes sequencing (CITE-seq) analysis to investigate the impact of granulocyte-colony stimulating factor on CRISPR/Cas9 gene edited human hematopoietic stem cell function

ABSTRACT: Our research has demonstrated that G-CSF impedes engraftment of CRISPR-Cas9 gene edited human hematopoietic stem cells (HSCs) by exacerbating p53-mediated DNA damage response. Results in this study suggest that the potential for G-CSF to exacerbate HSC toxicity mediated by DNA-damaging nucleases should be considered in autologous HSC gene therapy clinical trials.

ORGANISM(S): Homo sapiens

PROVIDER: GSE230182 | GEO | 2023/06/30

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Transcription profiling time series of mouse bone marrow macrophages treated with macrophage colony stimulating factor or granulocyte colony stimulating factor

Project description:BM monocytes were treated with 20ug/ml of M-CSF (macrophage colony stimulating factor) or GM-CSF (granulocyte monocyte colony stimulating factor) for 0, 6, 12 hours before harvesting RNA for analysis

2008-11-01 | E-MEXP-1803 | biostudies-arrayexpress

Murine Bone Marrow Stromal Cell Response to Granulocyte Colony-Stimulating Factor

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

Transcriptional profiling of human macrophages differentiated with macrophage colony-stimulating factor (M-CSF) and/or granulocyte-macrophage colony-stimulating factor (GM-CSF)

Project description:In this study, we compared human monocytes differentiated for 7 days with M-CSF and/or GM-CSF. A comparison of the different macrophage populations was made using microarray profiling. Threshold: 1.0 . Logbase: 2 . Technology: Agilent.SingleColor.14850. Normalization: Shift to 75 percentile . Baseline Transformation: median of all samples . FlagSettings:. Feature is not Uniform:A. Feature is a population outlier:A. Feature is Saturated:A. Feature is not above background:M. Feature is not positive and significant:M.

2012-03-20 | E-MTAB-791 | biostudies-arrayexpress

Murine Bone Marrow Stromal Cell Response to Granulocyte Colony-Stimulating Factor

2010-07-14 | GSE22925 | GEO

Transcriptional profiling of murine bone marrow-derived macrophages differentiated with macrophage colony-stimulating factor (M-CSF) and/or granulocyte-macrophage colony-stimulating factor (GM-CSF) for short term

Project description:In this study, we compared murine bone marrow monocytes differentiated for 7 days with M-CSF then BMM were cultured in the absence of M-CSF for 24hr (starved), then treated with different combinations of M-CSF, GM-CSF, TNF and Dex for 16hr. A comparison of the different macrophage populations was made using microarray profiling. Threshold: 1.0 . Logbase: 2 . Technology: Agilent.SingleColor.14868. Normalization: Shift to 75 percentile . Baseline Transformation: median of all samples . FlagSettings:. Feature is not Uniform:A. Feature is a population outlier:A. Feature is Saturated:A. Feature is not above background:M. Feature is not positive and significant:M.

2012-03-20 | E-MTAB-792 | biostudies-arrayexpress

Granulocyte colony-stimulating factor reprograms bone marrow stromal cells to actively suppress B lymphopoiesis in mice

Project description:G-CSF treatment targets CXCL12-abundant reticular (CAR) cells to suppress their production of a number of B trophic factors, including CXCL12, IL-6, IL-7, IGF-1, and Flt3 ligand.

2015-03-21 | GSE67104 | GEO

Granulocyte-Colony Stimulating Factor reduces cocaine-seeking and downregulates glutamatergic synaptic proteins in medial prefrontal cortex

Project description:Abstract Background Psychostimulant use disorder is a major public health issue, and despite the scope of the problem there are currently no FDA approved treatments. There would be tremendous utility in development of a treatment that could help patients both achieve and maintain abstinence. Previous work from our group has identified granulocyte-colony stimulating factor (G-CSF) as a neuroactive cytokine that alters behavioral response to cocaine, increases synaptic dopamine release, and enhances cognitive flexibility. Here, we investigate the role of G-CSF in affecting extinction and reinstatement of cocaine-seeking and perform detailed characterization of its proteomic effects in multiple limbic substructures. Methods Sprague-Dawley rats were injected with PBS or G-CSF during (1) extinction or (2) abstinence from cocaine self-administration, and drug seeking behavior was measured. Quantitative assessment of changes in the proteomic landscape in the nucleus accumbens (NAc) and medial prefrontal cortex (mPFC) were performed via data-independent acquisition (DIA) mass spectrometry analysis. Results Administration of G-CSF during extinction accelerated the rate of extinction, and administration during abstinence attenuated cue-induced cocaine-seeking. Analysis of global protein expression demonstrated that G-CSF regulated proteins primarily in mPFC that are critical to glutamate signaling and synapse maintenance. Conclusion Taken together, these findings support G-CSF as a viable translational research target with the potential to reduce drug craving or seeking behaviors. Importantly, recombinant G-CSF exists as an FDA-approved medication which may facilitate rapid clinical translation. Additionally, using cutting-edge multi-region discovery proteomics analyses, these studies identify a novel mechanism underlying G-CSF effects on behavioral plasticity.

2021-01-28 | PXD019485 | Pride

Transcriptional profiling of murine bone marrow derived macrophages differentiated with macrophage colony-stimuating factor (M-CSF) or granulocyte-macrophage colony-stimulating factor (GM-CSF)

Project description:In this study, we compared murine bone marrow monocytes differentiated for 7 days with M-CSF or GM-CSF. A comparison of the different macrophage populations was made using microarray profiling. Threshold: 1.0 . Logbase: 2 . Technology: Agilent.SingleColor.14868. Normalization: Shift to 75 percentile . Baseline Transformation: median of all samples . FlagSettings:. Feature is not positive and significant:M. Feature is not above background:M. Feature is not Uniform:A. Feature is a population outlier:A. Feature is Saturated:A.

2012-03-20 | E-MTAB-790 | biostudies-arrayexpress

Single-cell RNA sequencing characterizes the comparision between Granulocyte-colony stimulating factor (G-CSF) primed human bone marrow and unstimulated bone marrow

Project description:Purpose: The goal of the study is to obatin a comprehensive landscape of G-CSF primed bone marrow (G-BM) and to deciphering the underlying mechanisms of immune modulatory effect induced by G-CSF treatment. Methods: We recruited two healthy donors and treated them with recombinant G-CSF at a dosage of 5μg/kg body weight per day for 5 consecutive days. The bone marrow samples were collected by aspiration on the fourth day of G-CSF treatment. Bone marrow samples from healthy donors were treated with lysing solution to remove erythrocytes and were then labeled with antibodies. Through flow sorting, the final cells used for single-cell RNA sequencing (scRNA-seq) contained CD45+CD66b- population (90%), CD66b+ population (5%), and CD45- population (5%). Results and Conclusion: Through unbiased analysis, our data systematically showed the alterations in the transcriptional landscape of hematopoietic cells in G-BM, and illustrated the mechanisms of hyporesponsiveness of T cells and natural killer (NK) cells caused by G-CSF stimulation.

2022-06-23 | GSE193138 | GEO

RUNX1 haploinsufficiency results in granulocyte colony-stimulating factor hypersensitivity.

Project description:RUNX1/AML1 is among the most commonly mutated genes in human leukemia. Haploinsufficiency of RUNX1 causes familial platelet disorder with predisposition to myeloid malignancies (FPD/MM). However, the molecular mechanism of FPD/MM remains unknown. Here we show that murine Runx1(+/-) hematopoietic cells are hypersensitive to granulocyte colony-stimulating factor (G-CSF), leading to enhanced expansion and mobilization of stem/progenitor cells and myeloid differentiation block. Upon G-CSF stimulation, Runx1(+/-) cells exhibited a more pronounced phosphorylation of STAT3 as compared with Runx1(+/+) cells, which may be due to reduced expression of Pias3, a key negative regulator of STAT3 signaling, and reduced physical sequestration of STAT3 by RUNX1. Most importantly, blood cells from a FPD patient with RUNX1 mutation exhibited similar G-CSF hypersensitivity. Taken together, Runx1 haploinsufficiency appears to predispose FPD patients to MM by expanding the pool of stem/progenitor cells and blocking myeloid differentiation in response to G-CSF.

| S-EPMC4742622 | biostudies-literature

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data