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IL-1 receptor antagonist prevents bias to myelopoiesis in hematopoietic stem cells and protects from neoplasia

ABSTRACT: IL-1 receptor antagonist prevents bias to myelopoiesis in hematopoietic stem cells and protects from neoplasia

PROVIDER: PRJNA522750 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8582230_1.fastq.gz	Fastqsanger.gz
	SRR8582230_2.fastq.gz	Fastqsanger.gz
	SRR8582240_1.fastq.gz	Fastqsanger.gz
	SRR8582240_2.fastq.gz	Fastqsanger.gz
	SRR8582231_1.fastq.gz	Fastqsanger.gz

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IL-1 receptor antagonist prevents bias to myelopoiesis in hematopoietic stem cells and protects from neoplasia

Project description:IL-1 receptor antagonist prevents bias to myelopoiesis in hematopoietic stem cells and protects from neoplasia

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IL-1 receptor antagonist prevents bias to myelopoiesis in hematopoietic stem cells and protects from neoplasia

Project description:Interleukin-1β (IL-1β) drives hematopoietic stem cell (HSC) differentiation into the myeloid lineage, and enhanced IL-1β signaling plays a key role in hematological malignancies. However, little is known on the role of its endogenous regulatory cytokine, IL-1 receptor antagonist (IL-1rn), on both healthy and malignant hematopoiesis. Here, we show that inflammation through unbalanced IL-1rn is present in the experimental model of acute myeloid leukemia (AML) driven by the NRAS-G12D oncogene.

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IL-1 receptor antagonist prevents bias to myelopoiesis in hematopoietic stem cells and protects from neoplasia

Project description:Interleukin-1β (IL-1β) drives hematopoietic stem cell (HSC) differentiation into the myeloid lineage, and enhanced IL-1β signaling plays a key role in hematological malignancies. However, little is known on the role of its endogenous regulatory cytokine, IL-1 receptor antagonist (IL-1rn), on both healthy and malignant hematopoiesis. Here, we show that in vivo genetic deletion of IL-1rn induces HSC differentiation into the myeloid lineage and hampers B cell development. It also causes damage to the Stromal Compartment of the Bone Marrow.

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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.

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Dye Bias Array Set

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