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Perivascular niche cells sense thrombocytopenia and activate platelet-biased HSCs in an IL-1 dependent manner

ABSTRACT: Perivascular niche cells sense thrombocytopenia and activate platelet-biased HSCs in an IL-1 dependent manner

PROVIDER: PRJNA496483 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8056590.fastq.gz	Fastqsanger.gz
	SRR8056600.fastq.gz	Fastqsanger.gz
	SRR8056610.fastq.gz	Fastqsanger.gz
	SRR8056620.fastq.gz	Fastqsanger.gz
	SRR8056630.fastq.gz	Fastqsanger.gz

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Perivascular niche cells sense thrombocytopenia and activate platelet-biased HSCs in an IL-1 dependent manner

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Project description:Although bone marrow (BM) niche cells are essential for hematopoietic stem cell (HSC) maintenance, their interaction in response to stress is not well defined. Here, we used a mouse model of acute thrombocytopenia to investigate the crosstalk between HSCs and niche cells during restoration of the thrombocyte pool. This process required membrane-localized stem cell factor (m-SCF) in megakaryocytes, which was regulated by vascular endothelial growth factor A (VEGF-A) and platelet-derived growth factor-B (PDGF-B) derived from BM endothelial cells. HSCs and multipotent progenitors 2 (MPP2), but not MPP3/4 were subsequently activated by a dual receptor tyrosine kinase (RTK)-dependent signaling event, namely m-SCF/c-Kit and VEGF-A/VEGFR-2, contributing to their selective and early proliferation. Our findings describe a dynamic network of signals in response to the acute loss of a single blood cell type, and reveal the important role of three RTKs in orchestrating the selective activation of HSCs and progenitor cells in thrombocytopenia.

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Perivascular niche cells sense thrombocytopenia and activate hematopoietic stem cells in an IL-1 dependent manner.

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Effect of bioengineered niches on perivascular stem cell phenotype.

Project description:Long-term reconstituting haematopoietic stem cells (LT-HSCs) are used to treat blood disorders via allogeneic stem cell transplantation (alloSCT), to engraft and repopulate the blood system. The very low abundance of LT-HSCs and their rapid differentiation during in vitro culture hinders their clinical utility. Previous developments using stromal feeder layers, defined media cocktails, and bioengineering have enabled HSC expansion in culture, but of mostly short-term HSCs (ST-HSC) and progenitor populations at the expense of naïve LT-HSCs. Here, we report the creation of a bioengineered LT-HSC maintenance niche that recreates physiological extracellular matrix organisation, using soft collagen type-I hydrogels to drive nestin expression in perivascular stromal cells (PerSCs or pericytes). We demonstrate that nestin, which is expressed by HSC-supportive bone marrow stromal cells, is cytoprotective and, via regulation of metabolism, is important for HIF-1 expression in PerSCs. When CD34+ve HSCs were added to the bioengineered niches comprising nestin/HIF-1 expressing PerSCs, LT-HSC numbers were maintained with normal clonal and in vivo reconstitution potential, without media supplementation. We provide proof-of-concept that our bioengineered niches can support the survival of CRISPR edited HSCs. Successful editing of LT-HSCs ex vivo can have potential impact on the treatment of blood disorders.

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Project description:Hematopoietic stem cells (HSCs) display heritable and deterministic gene regulatory states associated with functional heterogeneity. However how these biased fate programs change through development remains poorly understood. Here, using single-cell lineage tracing, we map the function and state of thousands of individual mouse HSCs spanning from the earliest mature fetal stages until young adults. We identify a burst of platelet- and myeloid-biased HSCs during the first postnatal week. Fetal HSCs retain a fetal-like program even after 4 months in the recipient bone marrow, suggesting that the adult HSC program is epigenetically configured early after birth. Creating a single-cell atlas of mouse perinatal HSCs, we identify a transient HSC state with hallmarks of Epithelial-Mesenchymal Transition (EMT), mTOR complex 1 activity, and cholesterol synthesis (SREBP targets). Tracing the rare cells that traverse this transient state, we reveal the neonatal origin of long-term platelet/myeloid-biased HSCs in both native and transplantation hematopoiesis. Transient treatment with mTORC1 inhibitor rapamycin during the first postnatal week suffices to reduce the platelet-biased adult HSC programming, without affecting total HSC numbers. In sum, we reveal a late developmental origin for platelet-biased HSCs, with important implications for hematopoietic aging.

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