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Myeloid-biased HSC require Semaphorin 4A from the bone marrow niche for self-renewal under stress and life-long persistence

ABSTRACT: Myeloid-biased HSC require Semaphorin 4A from the bone marrow niche for self-renewal under stress and life-long persistence

PROVIDER: PRJEB61862 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR11344955_1.fastq.gz	Fastqsanger.gz
	ERR11344955_2.fastq.gz	Fastqsanger.gz
	ERR11344956_1.fastq.gz	Fastqsanger.gz
	ERR11344956_2.fastq.gz	Fastqsanger.gz
	ERR11344957_1.fastq.gz	Fastqsanger.gz

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Myeloid-biased HSC require Semaphorin 4A from the bone marrow niche for self-renewal under stress and life-long persistence

Project description:Tissue stem cells are hierarchically organized, but the signals that selectively preserve their functional integrity are largely unknown. Semaphorin 4A (Sema4A) is a specific regulator of myeloid-biased hematopoietic stem cells (myHSC), which are positioned at the top of the HSC hierarchy. Through single-cell transcriptomics, we compare the effect of Sema4A knock-out on the myHSCs.

2023-06-04 | E-MTAB-12890 | biostudies-arrayexpress

Myeloid-biased HSC require Semaphorin 4A from the bone marrow niche for self-renewal under stress and life-long persistence

2022-01-21 | E-MTAB-11359 | biostudies-arrayexpress

Myeloid-biased HSC require Semaphorin 4A from the bone marrow niche for self-renewal under stress and life-long persistence

Project description:Tissue stem cells are hierarchically organized. Those that are most primitive serve as key drivers of regenerative response but the signals that selectively preserve their functional integrity are largely unknown. Here, we identify a secreted factor, Semaphorin 4A (Sema4A), as a specific regulator of myeloid-biased hematopoietic stem cells (myHSC), which are positioned at the top of the HSC hierarchy. Lack of Sema4A leads to exaggerated myHSC (but not downstream “balanced” HSC) proliferation after acute inflammatory stress, indicating that Sema4A enforces myHSC quiescence. Strikingly, aged Sema4A knock-out myHSC expand but almost completely lose reconstitution capacity. The effect of Sema4A is non cell-autonomous, since upon transplantation into Sema4A-deficient environment, wild-type myHSC excessively proliferate but fail to engraft long-term. Sema4A constrains inflammatory signaling in myHSC and acts via a surface receptor Plexin-D1. Our data support a model whereby the most primitive tissue stem cells critically rely on a dedicated signal from the niche for self-renewal and life-long persistence.

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Myeloid-biased HSC require Semaphorin 4A from the bone marrow niche for self-renewal under stress and life-long persistence

Project description:Myeloid-biased HSC require Semaphorin 4A from the bone marrow niche for self-renewal under stress and life-long persistence

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Myeloid-biased HSC require Semaphorin 4A from the bone marrow niche for self-renewal under stress and life-long persistence

Project description:Myeloid-biased HSC require Semaphorin 4A from the bone marrow niche for self-renewal under stress and life-long persistence

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Bulk and single RNA sequencing on the role of Igf2bp2 in myeloid-biased HSC

Project description:Using RNA sequencing analysis on myeloid biased HSC, we compared gene expression profiles between WT and Igf2bp2 knock-out mice at young and old age. 1421 differentially expressed genes were identified in young myeloid biased HSC from Igf2bp2 knock-out mice compared to young WT; however, only 26 differentially expressed genes were identified in old myeloid biased HSC from Igf2bp2 knock-out mice compared to old WT. Compared to young WT myeloid biased HSC, myeloid biased HSC from young Igf2bp2 knock-out exhibits reduced expression of genes involved in metabolism and translation. In addition, single cell RNA sequencing analysis of myeloid biased HSC in young wildtype mice identified nine sub-clusters. HSCs from a sub-cluster with high expression of Igf2bp2 exhibit up-regulated IGF/PI3K/AKT signaling and increased expression of genes involved in HSC quiescence and maintenance. Altogether, the study provides a correlation and mechanism to understand the role of Igf2bp2 in HSC function and aging.

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