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Regulation of the hematopoietic stem cell pool by c-Kit-associated trogocytosis

ABSTRACT: Regulation of the hematopoietic stem cell pool by c-Kit-associated trogocytosis

PROVIDER: PRJNA1112308 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29049531_1.fastq.gz	Fastqsanger.gz
	SRR29049531_2.fastq.gz	Fastqsanger.gz
	SRR29049532_1.fastq.gz	Fastqsanger.gz
	SRR29049532_2.fastq.gz	Fastqsanger.gz
	SRR29049533_1.fastq.gz	Fastqsanger.gz

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Regulation of the hematopoietic stem cell pool by c-Kit-associated trogocytosis

Project description:Hematopoietic stem cells (HSCs) are routinely mobilized from the bone marrow (BM) to the blood circulation for clinical transplantation. However, the mechanisms by which HSCs exit the marrow are not well understood. We found that most BM HSCs present the macrophage marker F4/80 on their cell surface. Upon enforced mobilization induced by granulocyte-colony-stimulating factor or CXCR4 antagonist, F4/80+ HSCs were selectively retained in the BM while F4/80— HSCs were mobilized to the blood. Remarkably, F4/80 was acquired through direct transfer via c-Kit-mediated trogocytosis from BM resident macrophages in mouse and human settings. Our study uncovers a function for BM-resident macrophages in controlling the HSC mobilizable pool, and identifies mechanisms that may be used to improve HSC yield for transplantation.

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Regulation of the hematopoietic stem cell pool by C-Kit-associated trogocytosis.

Project description:Hematopoietic stem cells (HSCs) are routinely mobilized from the bone marrow (BM) to the blood circulation for clinical transplantation. However, the precise mechanisms by which individual stem cells exit the marrow are not understood. This study identified cell-extrinsic and molecular determinants of a mobilizable pool of blood-forming stem cells. We found that a subset of HSCs displays macrophage-associated markers on their cell surface. Although fully functional, these HSCs are selectively niche-retained as opposed to stem cells lacking macrophage markers, which exit the BM upon forced mobilization. Macrophage markers on HSCs could be acquired through direct transfer by trogocytosis, regulated by receptor tyrosine-protein kinase C-Kit (CD117), from BM-resident macrophages in mouse and human settings. Our study provides proof of concept that adult stem cells utilize trogocytosis to rapidly establish and activate function-modulating molecular mechanisms.

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Project description:In vertebrates, lifelong supply of all the blood cell types in suitable numbers is maintained by the hematopoietic stem cells (HSCs). During development, these HSCs emerge in the aorta-gonad-mesonephros (AGM) from specialized vascular endothelium through a transdifferentiation process, called as endothelial-to-hematopoietic transition (EHT). During this process, select endothelial cells (CD31+c-kit- or CD31PCKITN) switch to a hematopoietic transcriptional program, undergo morphological changes and become hemogenic (CD31+c-kit+ or CD31PCKITP) and gives rise to hematopoietic cells (CD31-c-kit+ or CD31NCKITP). A complex interplay of key transcription factors and signaling pathways coordinates the whole process. Specific metabolic signature of a cell can precisely define its phenotype. Evidence has emerged that cellular phenotype and function can be driven according to the changes in cellular metabolism. Metabolic programs, which are stage specific, allow stem cells to adapt their function in different microenvironments. In the present study, we performed nano LC-MS/MS based proteomic analysis to understand the molecular program involved in the transdifferentiation of endothelial to hematopoietic cells.

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