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Next Generation Sequencing Analysis of Bone Marrow Hematopoietic Progenitor Cells (HPC) and Leukemic Progenitors (LP) Transcriptomes

ABSTRACT: Next Generation Sequencing Analysis of Bone Marrow Hematopoietic Progenitor Cells (HPC) and Leukemic Progenitors (LP) Transcriptomes

PROVIDER: PRJNA493124 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7903020_1.fastq.gz	Fastqsanger.gz
	SRR7903020_2.fastq.gz	Fastqsanger.gz
	SRR7903021_1.fastq.gz	Fastqsanger.gz
	SRR7903021_2.fastq.gz	Fastqsanger.gz
	SRR7903022_1.fastq.gz	Fastqsanger.gz

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Next Generation Sequencing Analysis of Bone Marrow Hematopoietic Progenitor Cells (HPC) and Leukemic Progenitors (LP) Transcriptomes

Project description:Purpose: Next Generation Sequencing Analysis has revolutionized systems-based analysis of cellular pathways. The goals of this study are to compare the transcriptomes between bone marrow HPC and LP sorted from early phase (E) and median phase (M) to find the changed genes in LP.

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Human RORγt+ CD34+ cells are lineage-specified progenitors of group 3 RORγt+ innate lymphoid cells

Project description:Group 3 innate lymphoid cells (ILC3) are defined by the expression of RORγt, which is selectively required for their development. The lineage-specified progenitor cells of human ILC3 and their developmental site after birth remain undefined. Here we identified a novel population of human CD34+ hematopoietic progenitor cells (HPC) expressing RORγt and sharing with ILC3 a distinct transcriptional signature. RORγt+ CD34+ HPC were located in tonsils and intestinal lamina propria (LP) and selectively differentiated towards ILC3. Conversely, RORγt- CD34+ HPC displayed commitment potential for both ILC3 and NK cells and the differentiation fate towards these two cell lineages was determined by cytokine and aryl hydrocarbon receptor (AhR) signaling. Thus, we propose that RORγt+ CD34+ cells represent human lineage-specified progenitors of IL-22+ ILC3 and that tonsils as well as intestinal LP might be preferential sites of their differentiation.

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Human RORM-NM-3t+ CD34+ cells are lineage-specified progenitors of group 3 RORM-NM-3t+ innate lymphoid cells

Project description:Group 3 innate lymphoid cells (ILC3) are defined by the expression of RORM-NM-3t, which is selectively required for their development. The lineage-specified progenitor cells of human ILC3 and their developmental site after birth remain undefined. Here we identified a novel population of human CD34+ hematopoietic progenitor cells (HPC) expressing RORM-NM-3t and sharing with ILC3 a distinct transcriptional signature. RORM-NM-3t+ CD34+ HPC were located in tonsils and intestinal lamina propria (LP) and selectively differentiated towards ILC3. Conversely, RORM-NM-3t- CD34+ HPC displayed commitment potential for both ILC3 and NK cells and the differentiation fate towards these two cell lineages was determined by cytokine and aryl hydrocarbon receptor (AhR) signaling. Thus, we propose that RORM-NM-3t+ CD34+ cells represent human lineage-specified progenitors of IL-22+ ILC3 and that tonsils as well as intestinal LP might be preferential sites of their differentiation. ILC3, NK cells and the CD34+ HPC subsets were sorted from tonsils of 6 distinct donors to purity above 95%. cRNA of the sorted cell populations was hybridized to an Agilent Whole Human Genome Oligo Microarrays (8x60K v2, Design ID 039494)

2014-11-25 | E-GEOD-63197 | biostudies-arrayexpress

Pre-leukemic Cebpa mutant myeloid progenitors

Project description:In this study, we use pre-malignant cells from different Cebpa mutant acute myeloid leukemia (AML) models. We have used conditional KO models (CreLoxP) and isolated hematopoietic cells shortly after induction of recombination, in order to look at pre-leukemic cells, which have acquired the first hit, but not yet undergone full malignant transformation. We have sorted granulocyte-macrophage progenitors (GMPs) and the more immature population pre-granulocyte-macrophages (preGMs) from pre-leukemic mice. We analyzed gene-expression profiles in order to find deregulated genes, which make the cells more prone to undergo transformation.

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Profiling of the chromatin landscape of hematopoietic progenitor cells (HPC) transduced with transcription factors T-BET and EOMES [ATAC-seq HPC]

Project description:T-BET and EOMES are key transcription factors in the development of mature Natural Killer (NK) cells in mice. However, the role of these transcription factors during human NK cell development is less well understood. Therefore, we overexpressed T-BET or EOMES in human umbilical cord blood-derived HPC and cultured them in vitro in an NK cell differentiation model. To evaluate the effect of early overexpression of T-BET and EOMES in HPC, the chromatin landscape was uncovered using assay for transposase-accessible chromatin (ATAC) sequencing. In this way, the regulatory effect of T-BET and EOMES overexpression on the epigenome of HPC was evaluated.

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Project description:ObjectiveFaster engraftment of G-CSF-mobilized peripheral blood (MPB) transplants compared to steady-state bone marrow (ssBM) is well documented and clinically relevant. A number of different factors likely contribute to this outcome. In the present study we explored whether independent of cell number there are intrinsic differences in the efficiency of progenitor cell homing to marrow between MPB and ssBM.MethodsMobilization was achieved by continuous infusion of G-CSF alone or in combination with other mobilizing agents. In vivo homing assays, in vitro migration assays, gene expression analysis, and flow cytometry were utilized to compare homing-related in vivo and in vitro properties of MPB and ssBM HPC.ResultsMarrow homing of murine MPB HPC, generated by different mobilizing schemes, was reproducibly significantly superior to that of ssBM, in lethally irradiated as well as in nonirradiated hosts. This phenotype was independent of MMP9, selectins, and beta2- and alpha4-integrins. Superior homing was also observed for human MPB HPC transplanted into NOD/SCIDbeta2microglobulin(-/-) recipients. Inhibition of HPC migration abrogated the homing advantage of MPB but did not affect homing of ssBM HPC, whereas enhancement of motility by CD26 inhibition improved marrow homing only of ssBM HPC. Enhanced SDF-1-dependent chemotaxis and low CD26 expression on MPB HPC were identified as potential contributing factors. Significant contributions of the putative alternative SDF-1 receptor, RDC1, were unlikely based on gene expression data.ConclusionThe data suggest increased motility as a converging endpoint of complex changes seen in MPB HPC which is likely responsible for their favorable homing.

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Transcriptome profiling of hematopoietic progenitor cells (HPC) transduced with transcription factors T-BET or EOMES

Project description:T-BET and EOMES are key transcription factors in the development of mature Natural Killer (NK) cells in mice. However, the role of these transcription factors during human NK cell development is less well understood. Therefore, we overexpressed T-BET or EOMES in human umbilical cord blood-derived HPC and cultured them in vitro in an NK cell differentiation model. To evaluate the effect of early overexpression of T-BET and EOMES in HPC, transcriptome profiling was performed on T-BET and EOMES overexpressing HPC and compared to control transduced HPC by RNA sequencing on day 0 of culture.

2021-08-27 | GSE166437 | GEO

Transcriptomic profiling of LP lesions, hypertrophic LP (HLP) lesions, and healthy controls

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Human Hematopoietic Stem Cell (HSC) and Progenitor Cell (HPC) Expression Profilies

Project description:The global gene expression profiles of human umbilical cord blood and adult bone marrow CD34+CD33-CD38-Rho(lo)c-kit+ cells, enriched for hematopoietic stem/progenitor cells (HSC) with CD34+CD33-CD38-Rho(hi) cells, enriched in committed hematopoietic progenitor cells (HPC), were compared to identify candidate regulators of HSC self-renewal versus differentiation fate decisions. Keywords: parallel sample

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The signaling axis atypical protein kinase C l/i-Satb2 mediates leukemic transformation of B-cell progenitors

Project description:Oncogene driven transformation of leukemic progenitors results in B-acute lymphoblastic leukemia. Genetic deletions at specific hotspots are driven by recombination of epigenetically repressed loci and cause B cell transformation, and epigenetically regulated transcriptional plasticity has been proposed as a mechanism of differentiation arrest and resistance to therapy. The upstream signals driving epigenetic silencing have not been elucidated. BCR-ABL leukemias are initiated by leukemic stem cells/progenitors, and their modeling in vivo represents an opportunity for the identification of the epigenetic progress contributing to lineage leukemogenesis. We have found that primary human and murine BCR-ABL+ leukemic progenitors have increased activation of Cdc42 and the downstream atypical protein kinase C (aPKC). While the isoform aPKCz behaves as a leukemic suppressor, aPKCl/i is critically required for oncogenic progenitor proliferation, survival, and B cell differentiation arrest, but not for normal B cell lineage differentiation. We found that in vitro and in vivo B cell transformation by BCR-ABL requires the downregulation of key genes in the B-cell differentiation program through an aPKCl/i-dependent Etv5/Satb2 chromatin repressive signaling complex. Thus genetic or pharmacological targeting of aPKC impairs human oncogenic addicted leukemias in vitro and in vivo. Therefore, the aPKCl/i-SATB2 signaling cascade is required for leukemic BCR-ABL+ B-cell progenitor transformation and is amenable to non-BCR-ABL kinase inhibition.

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