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

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

PROVIDER: PRJNA795098 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17465152_1.fastq.gz	Fastqsanger.gz
	SRR17465152_2.fastq.gz	Fastqsanger.gz
	SRR17465153_1.fastq.gz	Fastqsanger.gz
	SRR17465153_2.fastq.gz	Fastqsanger.gz
	SRR17465154_1.fastq.gz	Fastqsanger.gz

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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.

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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.

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Small RNA sequencing of bone marrow extracellular vesicle labeled Granulocyte macrophage progenitors (GMPs) [GMP.sRNA]

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