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Breast cancer remotely imposes a myeloid bias on hematopoietic stem cells by reprogramming the bone marrow niche

ABSTRACT: Breast cancer remotely imposes a myeloid bias on hematopoietic stem cells by reprogramming the bone marrow niche

PROVIDER: PRJNA1020812 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26165256_1.fastq.gz	Fastqsanger.gz
	SRR26165256_2.fastq.gz	Fastqsanger.gz
	SRR26165257_1.fastq.gz	Fastqsanger.gz
	SRR26165257_2.fastq.gz	Fastqsanger.gz
	SRR26165258_1.fastq.gz	Fastqsanger.gz

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Breast cancer remotely imposes a myeloid bias on hematopoietic stem cells by reprogramming the bone marrow niche

Project description:Increased number of circulating myeloid cells is a hallmark of several cancers, however it remains unclear how primary tumors impact on myelopoiesis. Here we show that non-metastatic breast tumors remotely instruct the fate of long-term hematopoietic stem cell (HSCLT) in the bone marrow. We found that HSCLT from tumor bearing mice acquire a myeloid bias persisting upon primary and secondary HSCLT transfer in lethally-irradiated tumor-free animals. By imaging the bone marrow HSC niche, we found that the tumor-bearing status is associated with increased physical interactions between mesenchymal stem/stromal cells (MSC) and HSCLT. Moreover, ex vivo co-culture experiments demonstrate that MSC isolated from tumor-bearing mice increase myeloid differentiation of HSCLT isolated from tumor free mice. In summary, our data reveal that breast cancer remotely promotes myelopoiesis at the earliest stages of hematopoietic differentiation in the bone marrow mesenchymal niche.

2023-09-30 | GSE243964 | GEO

Bone marrow niche

Project description:Bone marrow niche

| PRJNA429031 | ENA

Bone marrow neutropoiesis bias underlies inflammatory comorbidities

Project description:Bone marrow neutropoiesis bias underlies inflammatory comorbidities

| PRJNA991451 | ENA

ICAM-1 deficiency in the bone marrow niche impairs quiescence and repopulation of hematopoietic stem cells

Project description:The bone marrow niche plays a critical role in controlling the fate of hematopoietic stem cells (HSCs) by integrating intrinsic and extrinsic signals. However, the molecular events in the HSC niche remain to be investigated. Here, we report that intercellular adhesion molecule-1 (ICAM-1) maintains HSC quiescence and repopulation capacity in the niche. ICAM-1-deficient mice (ICAM-1-/-) displayed significant expansion of phenotypic long-term HSCs with impaired quiescence, as well as favors myeloid cell expansion. ICAM-1-deficient HSCs presented normal reconstitution capacity during serial transplantation; however, reciprocal transplantation experiments showed that ICAM-1 deficiency in the niche impaired HSCs quiescence and repopulation capacity. In addition, ICAM-1 deletion caused failure to retain HSCs in the bone marrow and changed the expression profile of stroma cell-derived factors, possibly representing the mechanism for defective HSCs in ICAM-1-/- mice. Collectively, these observations identify ICAM-1 as a regulator in the bone marrow niche.

2018-06-21 | GSE114836 | GEO

Bone marrow neutropoiesis bias underlies inflammatory comorbidities [multiomics]

Project description:Bone marrow neutropoiesis bias underlies inflammatory comorbidities [multiomics]

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Bone marrow neutropoiesis bias underlies inflammatory comorbidities [smart_seq2]

Project description:Bone marrow neutropoiesis bias underlies inflammatory comorbidities [smart_seq2]

| PRJNA991458 | ENA

Clu regulate myeloid bias in aged hematopoietic stem cells

Project description:Clu is upregulated in aged HSCs and its knockout diminishes the myeloid bias.

2025-05-06 | GSE275462 | GEO

Bone marrow neutropoiesis bias underlies inflammatory comorbidities [RNA-Seq]

Project description:Bone marrow neutropoiesis bias underlies inflammatory comorbidities [RNA-Seq]

| PRJNA991453 | ENA

Identification of a portal vessel-associated fetal liver hematopoietic stem cell niche

Project description:Whereas the cellular basis of the hematopoietic stem cell (HSC) niche in the bone marrow has been characterized, the nature of the fetal liver (FL) niche is not yet elucidated. We show that Nestin+NG2+ pericytes associate with portal vessels, forming a niche promoting HSC expansion. Nestin+NG2+ cells and HSCs scale during development with the fractal branching patterns of portal vessels, tributaries of the umbilical vein. After closure of the umbilical inlet at birth, portal vessels undergo a transition from Neuropilin-1+Ephrin-B2+ artery to EphB4+ vein phenotype, associated with a loss of peri-portal Nestin+NG2+ cells and emigration of HSCs away from portal vessels. These data support a model in which HSCs are titrated against a peri-portal vascular niche with a fractal-like organization enabled by placental circulation. Characterization of the transcriptome of fetal liver and adult bone marrow niche using RNA-seq

2015-12-03 | E-GEOD-72341 | biostudies-arrayexpress

Bone marrow neutropoiesis bias underlies inflammatory comorbidities [smart_seq2]

Project description:Local chronic inflammation exacerbates the prevalence and severity of associated distal organ comorbidities, causing catastrophic consequences for patients. However, the underlying mechanisms remain unclear. Here, we found that periodontitis increased the circulating pro-inflammatory neutrophils, which could be easily recruited to rheumatoid arthritis (RA) joints and aggravated articular destruction. Single-cell multiomics sequencing has revealed that periodontitis induces transcriptomic and epigenomic rewiring of hematopoietic stem and progenitor cells (HSPCs), which display skewed differentiation toward the neutrophil lineage, resulting in an increase in pro-inflammatory neutrophils. We further identified that periodontitis-elevated type I interferons are responsible for guiding the continuous neutropoiesis bias in the bone marrow. Resolution of periodontitis can reverse the differentiation bias of HSPCs and alleviate the progression of RA. This study indicated that neutropoiesis bias induces the progression of inflammatory comorbidities and emphasizes the necessity of controlling local chronic inflammation in the management of inflammatory comorbidities.

2025-05-12 | GSE236479 | GEO

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