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Impact of HSC-derived immune training on granulocyte/macrophage progenitor chromatin landscape

ABSTRACT: Impact of HSC-derived immune training on granulocyte/macrophage progenitor chromatin landscape

PROVIDER: PRJNA845805 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19580032_1.fastq.gz	Fastqsanger.gz
	SRR19580032_2.fastq.gz	Fastqsanger.gz
	SRR19580033_1.fastq.gz	Fastqsanger.gz
	SRR19580033_2.fastq.gz	Fastqsanger.gz
	SRR19580034_1.fastq.gz	Fastqsanger.gz

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Impact of HSC-derived immune training on granulocyte/macrophage progenitor gene expression

Project description:Impact of HSC-derived immune training on granulocyte/macrophage progenitor gene expression

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Impact of HSC-derived immune training on granulocyte/macrophage progenitor gene expression

Project description:Trained immunity occurs when inflammatory stimulation reprograms myeloid cells to have increased effector functions upon secondary stimulation. Interestingly, the secondary stimulation can occur well beyond the lifetime of an individual myeloid cell, thus memory of immune training must reside in the hematopoietic system. After showing that long-term hematopoietic stem cells (HSCLT) from mice treated with pristane for eight weeks generate trained macrophages, we sought to uncover mechanisms underlying the heritable trained immunity program in myeloid cells. To do this we transplanted HSCLT from pristane mice into congenic recipients, and after 18 weeks of engraftment sorted out donor derived granulocyte monocyte progenitors (GMP). We then analyzed the chromatin landscape and transcriptome using low input chromatin accessibility and transcriptomics sequencing (LiCAT-seq) which allows for the co-generation of RNA-seq and ATAC-seq libraries from the same cellular pool. With this approach we found a unique epigenetic phenotype of reduced chromatin accessibility at metabolic genes in GMP from pristane HSCLT, which resulted in reduced transcription of metabolic genes, leading to reduced metabolism in mature macrophages.

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Impact of HSC-derived immune training on granulocyte/macrophage progenitor chromatin landscape

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Transcription profiling of human HSC enriched population, common myeloid progenitors, granulocyte macrophage progenitors, megakaryocyte progenitors, and leukemia stem cells (leukemic-GMP) reveals MLL-AF9 transforms committed progenitors to leukemia stem cells by activation of a stem cell program (expt 2)

Project description:Leukemias and other cancers possess a rare population of cells capable of self-renewal, and eradication of these cancer stem cells is likely necessary for long-term cancer-free survival. Given that both normal and cancer stem cells are capable of self-renewal the extent to which cancer stem cells resemble normal tissue stem cells is a critical issue if targeted therapies are to be developed. We introduced the MLL-AF9 fusion protein encoded by the t(9;11)(p22;q23) found in human acute myelogenous leukemia (AML) into murine committed granulocyte-macrophage progenitors (GMP). The resultant leukemias contained cells with an immunophenotype similar to normal GMP that were highly enriched for leukemia stem cells (LSC). Detailed gene expression comparisons between normal hematopoietic stem cells (HSC), committed progenitors, and the LSC population demonstrated the LSC were globally more similar to the normal GMP than any other population. However, a subset of genes highly expressed in normal stem cells was re-activated in the LSC. These data demonstrate LSC can be generated from committed progenitors without widespread reprogramming of gene expression, and a leukemia self-renewal associated signature is activated in the process. Our findings define progression from normal hematopoietic progenitor to leukemia stem cell, and suggest that targeting a self-renewal program expressed in an abnormal context may be possible. Experiment Overall Design: A normal HSC enriched population, common myeloid progenitors, granulocyte macrophage progenitors, megakaryocyte progenitors, and leukemia stem cells (leukemic-GMP) were isolated and labeled RNA was hybridzed to Affymetrix microarrays

2008-06-12 | E-GEOD-3722 | biostudies-arrayexpress

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