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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: PRJEB52992 | ENA |

REPOSITORIES: ENA

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			Action	DRS
		Other
	ERR9751220.fastq.gz	Fastqsanger.gz
	ERR9751230.fastq.gz	Fastqsanger.gz
	ERR9751240.fastq.gz	Fastqsanger.gz
	ERR9751250.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.

2024-12-11 | GSE281145 | GEO

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

| PRJEB61862 | ENA

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

| PRJNA1182374 | ENA

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.

2021-02-05 | GSE166176 | GEO

Differential gene expression profiles between myeloid-biased and lymphoid-biased hematopoietic stem cells.

Project description:Array analysis of My-bi and Ly-bi HSC identifies candidate molecules for myeloid-bias. Collectively the data show that HSC in adults are largely epigenetically fixed in differentiation and self-renewal behavior. A direct examination of the epigenetic mechanisms that imprint HSC is difficult. However, an indirect way of assessing the effects of epigenetic imprinting is to look for the expressed gene programs of different types of HSC. Therefore, we performed an array analysis in collaboration with Dr. Michael Cooke. My-bi and Ly-bi HSC were identified in clonally repopulated hosts. The analysis returned 218 differentially expressed genes (M-bM-^IM-% Log2 M-bM-^IM-%2, p< 0.05) of which 36 were found to be overexpressed in My-bi HSC and the rest was overexpressed in Ly-bi HSC (Appendix A). There was no difference in expression levels for genes known to be involved in fate decisions during differentiation. This agrees well with our data that lineage bias is a stable function of a HSC, and does not reflect a differentiated type of cell. Gene expression profiles of myeloid-biased (My-bi) and lymphoid-biased (Ly-bi) stem cells were analyzed. Clonally repopulated hosts were generated by limiting dilution of bone marrow into ablated hosts and lineage bias was determined. Single My-bi (Tenor) and Ly-bi (Mort) repopulated hosts were sacrificed and Donor type HSC were enriched for Sca-1+, Lin- cells. Two technical replicates of RNA extract were run from each clone.

2013-05-01 | E-GEOD-41702 | biostudies-arrayexpress

Gene expression profiles of Semaphorin 3G stimulated macrophages [RNA-seq]

Project description:Although Semaphorin 3G has some roles in the development of vessels, the roles in immune system are not characterized. We aimed to study how Semaphorin 3G affects the function of macrophages.

2022-05-17 | GSE176438 | GEO

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

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

| PRJNA699541 | ENA

Hhex regulates HSC self-renewal and stress hematopoiesis via repression of Cdkn2a

Project description:The Hematopoietically-expressed homeobox transcription factor (Hhex) is important for the maturation of definitive hematopoietic progenitors and B-cells during development. We have recently shown that in adult hematopoiesis, Hhex is dispensable for maintenance of hematopoietic stem cells (HSCs) and myeloid lineages but essential for the commitment of Common Lymphoid Progenitors (CLPs) to lymphoid lineages. However, whether Hhex plays a role in HSC self-renewal and myeloid expansion during hematopoietic stress is unknown. Here we show that during serial bone marrow transplantation, Hhex-deleted HSCs are progressively lost, revealing an intrinsic defect in HSC self-renewal. Moreover, Hhex-deleted mice show markedly impaired hematopoietic recovery following myeloablation. In vitro, Hhex-null blast colonies were incapable of replating, implying a specific requirement for Hhex in immature hematopoietic progenitors. Transcriptome analysis of Hhex-null Lin-Sca+Kit+ (LSK) cells showed that Hhex deletion leads to the deregulation of Polycomb Repressive Complex 2 (PRC2) target genes, including an upregulation of Cdkn2a locus, encoding the cell cycle repressors p16Ink4a and p19Arf. Indeed, loss of Cdkn2a restored Hhex-null blast colony replating in vitro, as well as hematopoietic reconstitution following myeloablation in vivo. Thus, HSCs require Hhex to repress Cdkn2a to enable continued self-renewal and response to hematopoietic stress.

2017-05-22 | GSE86209 | GEO

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