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Expression data from Lin- ckit+ FLT3+ hematopoietic stem and progenitor cells isolated from Cebpa wildtype and Cebpa knockout mice after FLT3L stimulation

ABSTRACT: Expression data from Lin- ckit+ FLT3+ hematopoietic stem and progenitor cells isolated from Cebpa wildtype and Cebpa knockout mice after FLT3L stimulation

PROVIDER: PRJNA609987 | ENA |

REPOSITORIES: ENA

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Expression data from Lin- ckit+ FLT3+ hematopoietic stem and progenitor cells isolated from Cebpa wildtype and Cebpa knockout mice after FLT3L stimulation

Project description:Cebpa is a gene known for its role in hematopoetic development. Though it is proven to be indispensible in myelopoesis, the details of the role played by Cebpa in dendritic cell development is fairly unknown. Steady state DC development can be modelled in vitro by treating Lin- HSPC with FLT3L. We used microarrays to analyse the genetic landscape of lin- cKit+ FLT3+ HSPC isolated from both Cebpa wildtype and Cebpa knockout mice before and after stimulation with FLT3L for 4 hours.

2020-06-17 | GSE146288 | GEO

Gene expression in WT, Flt3 KO, and Flt3L KO cDC1s and cDC2s

Project description:The goal of this study was to determine whether there are any gene expression changes in cDC1s and cDC2s from WT, Flt3 KO, or Flt3L KO mice. Specifically whether developing in the absence of Flt3 signaling had any effects on the gene expression of the cDCs

2018-02-20 | GSE110789 | GEO

The clonal and molecular aetiology of Flt3L-mediated ‘emergency’ dendritic cell development

Project description:Flt3 ligand (Flt3L) promotes an increased generation of type 1 conventional dendritic cells (cDC1s), resulting in enhanced immunity against infections and cancer. Here, we employ cellular barcoding to understand how Flt3L regulates single haematopoietic stem and progenitor cell (HSPC) fate. Our results demonstrate that although Flt3L stimulation can recruit some additional cDC1-generating HSPCs, the major contributing factor to higher cDC1 numbers is through enhanced clonal expansion. This selective cDC1 expansion occurs primarily via multi-/oligo-potent clones, without compromising their clonal output to other lineages. We then develop Divi-Seq to simultaneously profile division history, surface phenotype and the transcriptional state of single HSPCs during the early phase of the response. We discover that Flt3L-responsive HSPCs maintain a proliferative ‘early progenitor’-like state, which leads to a selective emergence of CD11c+cKit+ transitional precursors with high cellular output to cDC1s. These findings inform the mechanistic action of Flt3L in natural immunity and immunotherapy.

2020-04-03 | GSE147977 | GEO

Lin-sca1+cKit+ cells cultured with or without ILC2 supernatant

Project description:Lin-sca1+cKit+ cells cultured with or without ILC2 supernatant

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Gene epxression profiling in murine bone marrow Lin- cells transduced with BCR-ABL and/or IRF8 followed by Flt3L culture for 5 days

Project description:To understand the effect of BCR-ABL and IRF8 on gene expression pattern during in vitro dendritic cell differentiation, microarry analysis was performed. Murine bone marrow Lin- cells were transduced with retroviruses carrying human BCR-ABL cDNA and/or mouse Irf8 cDNA, and then cultured with Flt3L for 5 days. Two independent experiments were performed.

2013-11-15 | E-GEOD-44920 | biostudies-arrayexpress

Fms-like tyrosine kinase 3 (Flt3) contributes to a receptor tyrosine kinase signature regulating the cardiac side population

Project description:Fms-like tyrosine kinase 3 (Flt3) is a regulator of hematopoietic progenitor cells. It is a target of tyrosine kinase inhibitors (TKIs) used for acute myeloid leukemia treatment. Flt3 and its ligand (Flt3L) are expressed in the heart and cardiac side effects occur under Flt3-targeting TKIs. Whether Flt3/Flt3L also regulate cardiac progenitor cells (CPCs), however, is not known. The cardiac side population (SP) is a pool of heterogenous CPCs that can give rise to all cardiac lineages, hence contributing to cardiovascular homeostasis. Here we show that SP-CPCs produce and are responsive to Flt3L. Compared to wild-type, SP-CPCs from flt3L-/- mice are less abundant, with less contribution of CD45-CD34+ cells, and lower expression of gene sets related to epithelial-to-mesenchymal transition, cardiovascular development and stem cell differentiation. Upon culturing and compared to wild-type, flt3L-/- Sca1+CD31- SP-CPCs show increased proliferation and less vasculogenic commitment, but differentiation can be induced in the presence of receptor tyrosine kinase-activating growth factors. The observed differences are associated with decreased microvascularisation and global systolic function of flt3L-/- hearts. Thus, Flt3 contributes to a receptor tyrosine kinase signature necessary for the maintenance and functionality of SP-CPCs. These findings have potential implications regarding cardiovascular side effects observed under TKI therapy.

2021-11-30 | GSE168207 | GEO

Altered compensatory cytokine signaling underlies the discrepancy between Flt3-/- and Flt3l-/- mice

Project description:Altered compensatory cytokine signaling underlies the discrepancy between Flt3-/- and Flt3l-/- mice

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Gene expression in WT, Flt3 KO, and Flt3L KO cDC1s and cDC2s

Project description:Gene expression in WT, Flt3 KO, and Flt3L KO cDC1s and cDC2s

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Leukemia-associated activating mutation of Flt3 expands dendritic cells and alters T cell responses

Project description:One of the most common genetic alterations in acute myeloid leukemia is the internal tandem duplication (ITD) in the FLT3 receptor for cytokine FLT3 ligand (FLT3L). The constitutively active FLT3-ITD promotes the expansion of transformed progenitors, but also has pleiotropic effects on normal hematopoiesis. We analyzed the effect of FLT3-ITD on dendritic cells (DCs), which express FLT3 and can be expanded by FLT3L administration. We report that young pre-leukemic mice with the Flt3ITD knock-in allele manifest an expansion of all DCs including classical (cDCs) and plasmacytoid (pDCs). The expansion originated in DC progenitors, occurred in a cell-intrinsic manner and was further enhanced in Flt3ITD/ITD mice. The mutation caused the downregulation of Flt3 on the surface of DCs and reduced their responsiveness to Flt3L. Flt3ITD mice showed enhanced capacity to support T cell proliferation, including a cell-extrinsic expansion of regulatory T cells (Tregs). Accordingly, these mice restricted alloreactive T cell responses during graft-versus-host reaction, but failed to control autoimmunity in the absence of Tregs. Thus, the FLT3-ITD mutation directly affects DC development, thereby indirectly modulating T cell homeostasis and supporting Treg expansion. This effect of FLT3-ITD may subvert immunosurveillance and promote leukemogenesis in a cell-extrinsic manner.

2016-01-28 | GSE76132 | GEO

Transcription profiling of mouse LT-HSC hematopoietic stem cells from wild type and Cebpa knock-in mutant strains

Project description:Gene expression of LT-HSC (CD150+Flt3-lin-Sca-Kit+) hematopoietic stem cells from wild type mice was compared with LT-HSC from Cebpa knock-in mutant mice (K/L mutants). Fetal liver cells for each genotype were competitively transplanted into irradiant recipients. Donor-derived LT-HSC cells were isolated by FACS sorting of recipient bone marrow. Biological replicates of each (3 for wt, 2 for K/L) were generated and expression profiles were determined by hybridization to Affymetrix Moe430_2 arrays.

2009-11-03 | E-TABM-694 | biostudies-arrayexpress

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