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Next Generation RNA-Sequencing data of Hematopoietic stem cells and CML stem cells

ABSTRACT: To investigate why dipeptides accumulate in immature CML cells, we examined upstream gene expression patterns. We isolated the most primitive long-term stem cells, short-term stem cells, and KLS- progenitor cells from healthy littermate control and CML-affected mice and performed gene expression profiling using next-generation RNA-sequencing. Gene expression profiles of the most primitive long-term (LT) stem cells (CD150+CD48-CD135-KLS+ cells), short-term (ST) stem cells (CD150-CD48-CD135- KLS+ cells), and KLS- progenitor cells from healthy littermate control and CML-affected mice

ORGANISM(S): Mus musculus

SUBMITTER: Junil Kim

PROVIDER: E-GEOD-70031 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Next Generation RNA-Sequencing data of Hematopoietic stem cells and CML stem cells

Project description:To investigate why dipeptides accumulate in immature CML cells, we examined upstream gene expression patterns. We isolated the most primitive long-term stem cells, short-term stem cells, and KLS- progenitor cells from healthy littermate control and CML-affected mice and performed gene expression profiling using next-generation RNA-sequencing.

2015-09-18 | GSE70031 | GEO

Single cell RNA_Seq in aging of hematopoietic stem and progenitor cells

Project description:Here, we use single-cell RNA-Seq to examine variation between individual hematopoietic stem and progenitor cells from two mouse strains (C57BL/6 and DBA/2) as they age. We prepared libraries from long-term (LT-HSCs) (LSK CD150+CD48-), short-term hematopoietic stem cells (ST-HSCs) (LSK CD150-CD48-) and multipotent progenitors (MPPs) (LSK CD150+CD48+) from young (2-3 months) and old mice (22 months for C57BL/6 and 20 months for DBA/2). Population controls for each cell type and age were isolated by sorting processed in parallel.

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Functionally distinct subsets of lineage-biased multipotent progenitors control blood production in normal and regenerative conditions

Project description:To identify the molecular characterisitics of parallel lineage-biased MPP populations arising from hematopoietic stem cells (HSC) we conducted genome-wide analyses of hematopoietic stem, progenitor and mature myeloid cell populations using Affymetrix Gene ST1.0 arrays. Microarray analysis of 3-5 biological replicates of the indicated hematopoietic populations, isolated by FACS sorting from C57BL/6 mouse BM. Immunophenotypic definitions: Long-term HSC (HSCLT) (Lin-/cKit+/Sca1+/Flk2-/CD48-/CD150+); Short-term HSC (HSCST) (Lin-/cKit+/Sca1+/Flk2-/CD48-/CD150-); MPP2 (Lin-/cKit+/Sca1+/Flk2-/CD48+/CD150+); MPP3 (Lin-/cKit+/Sca1+/Flk2-/CD48+/CD150-); MPP4 (Lin-/cKit+/Sca1+/Flk2+); CMP (Lin-/cKit+/Fc?R-/CD34+); GMP (Lin-/cKit+/Fc?R+/CD34+); Pre-granulocyte (PreGr) (Mac1+/Gr1int); Granulocyte (Gr) (Mac1+/Gr1hi). HSC and GMP samples listed here were also used as controls for our related microarray study GSE48893.

2015-05-05 | E-GEOD-68529 | biostudies-arrayexpress

Fate mapping reveals two pathways of native thrombopoiesis (scRNA sequencing)

Project description:Transcriptomes of 1141 single cells isolated from bone marrow of induced R26rtTA/rtTA/Col1A1H2B-GFP/H2B-GFP mice; the following cell types were sorted: Megakaryocyte Progenitor (MkP): lineage- Sca-1- c-kit+ CD41+ CD150+; Multipotent Progenitor (MPP): lineage- Sca-1+ c-kit+ CD48- CD150- ; Hematopoietic Stem Cell (HSC):lineage- Sca-1+ c-kit+ CD48- CD150+; E34 HSC: lineage- Sca-1+ c-kit+ CD48- CD150+ CD201hi CD34-/lo; Restricted hematopoietic progenitor 1 (HPC-1): lineage- Sca-1+ c-kit+ CD48+ CD150-; lineage- kit+ CD41- CD150- cells; lineage- kit+ CD150+ cells.

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Project description:Murine hematopoietic stem cells were sorted by FACS from C57BL/6 Evi1+/GFP mice. Gene expression profiles of LSKCD41–CD48–CD150+CD34+ cells, LSKCD41–CD48–CD150+CD34–Evi1-GFP– cells, and LSKCD41–CD48–CD150+CD34–Evi1-GFP+ cells were generated.

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Controlling Genetic Heterogeneity in Gene-edited Hematopoietic Stem Cells by Single Cell Expansion

Project description:Gene editing using engineered nucleases frequently produces unintended genetic lesions in hematopoietic stem cells (HSCs). Gene-edited HSC cultures thus contain heterogenous populations, the majority of which either do not carry the desired edit or harbor unwanted mutations. In consequence, transplanting edited HSCs carries the risks of suboptimal efficiency and of unwanted mutations in the graft. Here, we present an approach for expanding gene-edited HSCs at clonal density, allowing for genetic profiling of individual clones before transplantation. We achieved this by developing a defined, polymer-based expansion system and identifying long-term expanding clones within the CD201+CD150+CD48-c-Kit+Sca-1+Lin-(KSL) population of pre-cultured HSCs. This dataset compares the gene expression in three different populations: (1) CD201+CD150+CD48-KSL (2) CD201+CD150+CD48+KSL and (3) CD201-KSL cells.

2023-07-19 | GSE232527 | GEO

HSC expression array

Project description:Increased expression of Kruppel like factor 7 (KLF7) is an independent predictor of poor outcome in pediatric acute lymphoblastic leukemia. The contribution of KLF7 to hematopoiesis has not been previously described. Herein, we characterized the effect on murine hematopoiesis of the loss of KLF7 and enforced expression of KLF7. Long-term multilineage engraftment of Klf7-/- cells was comparable to control cells, and self-renewal, as assessed by serial transplantation, was not affected. Enforced expression of KLF7 results in a marked suppression of myeloid progenitor cell growth and a loss of short- and long-term repopulating activity. Interestingly, enforced expression of KLF7, while resulting in multi-lineage growth suppression that extended to hematopoietic stem cells and common lymphoid progenitors, spared T cells and enhanced the survival of early thymocytes. RNA expression profiling of KLF7-overexpressing hematopoietic progenitors identified several potential target genes mediating these effects. Notably, the known KLF7 target Cdkn1a (p21Cip1/Waf1) was not induced by KLF7, and loss of CDKN1A does not rescue the repopulating defect. These results suggest that KLF7 is not required for normal hematopoietic stem and progenitor (HSPC) function, but increased expression, as seen in a subset of lymphoid leukemia, inhibits myeloid cell proliferation and promotes early thymocyte survival. HSC expression array: Lin- c-Kit+ Sca-1+ CD150+ CD48- CD41- cells were sorted from wild-type C57Bl/6 mice and RNA expression analyzed. RNA expression in KLS SLAM cells. KLS-SLAM cells were sorted from 6-10 week old C57Bl/6 mice

2012-08-24 | E-GEOD-40324 | biostudies-arrayexpress

Therapy resistant primitive stem cells in chronic myelogenous leukemia are characterized by low c-Kit expression and altered SCF response

Project description:Leukemia stem cells (LSC) in chronic myelogenous leukemia (CML) resist elimination with tyrosine kinase inhibitors (TKI) and persist as a source of disease recurrence. LSC populations are heterogeneous, but the most primitive, drug-resistant subsets are not well characterized. Previous studies indicate that variable cell-surface expression of the c-Kit receptor identifies heterogeneous hematopoietic stem cells (HSC) populations. We found that c-Kit expression is reduced on CML LSC compared to normal HSC. Long-term engraftment and leukemia generation capacity was restricted to low c-Kit expressing (c-KitLow) LSC, which showed increased quiescence and inflammatory gene signatures expression. The c-Kit ligand, stem cell factor (SCF), expanded normal HSC but drove maturation of CML LSC. The proportion of c-Kitlow LT-HSC was increased with TKI treatment. Supplementary SCF treatment enhanced elimination of committed but not primitive CML LT-HSC in TKI-treated mice. Low c-Kit expression identifies primitive, treatment-resistant LSC subpopulations with distinct regulatory characteristics, that are critical therapeutic targets.

2022-11-29 | GSE180496 | GEO

RNA-seq profiling of HSC, MPPs and HPC-1s from Phf6-deleted and Phf6-intact mice

Project description:The study profiled the effect of Phf6 deletion on gene expression in hematopoietic stem cells (HSCs), multipotent progenitor cells (MPPs) and hematopoietic progenitor cells (HPC-1). Phf6lox/Y;Tie2-creTg/+ mice were prepared on a C57BL/6 background so that Phf6 deletion could be selectively mediated by Tie2-cre. Cell populations were sorted from bone marrow samples using standard surface markers (Lin–SCA1+cKIT+(LSK) CD150+ CD48– for HSCs, Lin–SCA1+cKIT+(LSK) CD150– CD48– for MPPs and Lin–SCA1+cKIT+(LSK) CD150- CD48+ for HPC-1 cells). Phf6 intact and Phf6-delected cells of all three types were profiled by paired-end RNA-seq using an Illumina NextSeq 500 sequencer. RNA-seq libraries were prepared from the HPC-1 samples used a standard Illumina TruSeq library protocol whereas the libraries for the HSC and MPP samples used a SMART-seq ultra low input kit for cDNA synthesis and amplification. Statistical analysis of the TruSeq and SMART-seq samples was undertaken separately.

2019-02-20 | GSE126316 | GEO

Transcription profiling of human untreated and fenretinide-treated CD34+ cells from 4 CML patients

Project description:Imatinib therapy is first-line treatment for chronic myeloid leukemia (CML), and its failure to target CML progenitor/stem cells may lead to an increased risk of relapse. We report here that fenretinide, a well-tolerated vitamin A derivative, is capable of eradicating primitive CML progenitor/stem cells and significantly enhances the efficacy of imatinib at physiologically achievable concentrations. As tested by colony forming cell assays, formation of various colonies derived primitive CML CD34+ cells was significantly suppressed by fenretinide, particularly with respect to the formation of colonies derived from erythroid progenitors and more primitive CML progenitor/stem cells. Also, fenretinide significantly enhanced the ability of imatinib to suppress the formation of the colonies. Moreover, fenretinide was able to induce apoptosis in primitive CML CD34+ cells while sparing the normal counterparts. In particular, primitive CML CD34+CD38- cells appeared to be most sensitive to fenretinide induced apoptosis. Through transcriptome analysis and molecular validation, we further showed that fenretinide induced apoptosis in CML CD34+ cells was probably mediated by a series of stress responsive events which were likely triggered by elevated levels of intracellular reactive oxygen species. Accordingly, the combination of fenretinide and imatinib may provide a potential solution for overcoming relapse and resistance in CML. Experiment Overall Design: Transcriptome profiles of CML CD34+ cells with and without fenretinide treatment were analyzed using whole genome expression arrays (Affymetrix HG-U133 Plus 2.0) in four CML patients (CML32, CML33, CML34 and CML35, see Table 1). To minimize potential data biases, both treated and untreated cell samples were maintained in culture for 48 hours before hybridization.

2009-12-05 | E-GEOD-17480 | biostudies-arrayexpress

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