Transcriptomic analysis of wild type and Nr4a1-/- adipose progenitors.
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ABSTRACT:
PROVIDER: PRJNA487092 | ENA |
REPOSITORIES: ENA
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Project description:The project aims to identify differentially expressed genes in adipose progenitors that were freshly isolated from wild-type or Nr4a1-/- mice. The AP preparation involved adipose tissue digestion, and negative selection of the stromal vascular fraction (depletion of CD31+ endothelial cells and Lineage positive cells.
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Project description:We investigate the cellular and molecular mechanisms of tumor suppression by NR4A1 and NR4A3, and show a cell intrinsic essential function in maintenance of hematopoietic stem cell (HSC) homeostasis. In the absence of Nr4a1/3, HSC lost quiescence, became highly proliferative leukemia-stem cell (LSC) that transplanted AML to recipient mice. We further revealed that loss of NR4A1/3 leads to deregulated expression of the key cell cycle regulator Cdkn1c (P57), c-Myc oncogene, and glucose metabolic genes leading to enhanced aerobic glycolysis or Warburg effect in LSCs. Reintroduction of Nr4a1 in LSCs restored HSC quiescence, and reversed Nr4a1/3 deficiency induced P57 suppression and c-Myc overexpression. Collectively, we identify an essential role of Nr4a1/3 in coordinately regulating cell cycle entry and glucose metabolism to prevent uncontrolled stem cell proliferation and AML transformation. These results have major implications for designing therapeutic strategies in AML. To identify NR4A-dependent molecular signaling pathways that may control HSC homeostasis, we performed genome-wide transcript profiling of Lin-Sca1+ (LS) cells from WT and DKO mice. For Affymetrix analysis, we generated three independent pools of RNA from sorted LS cells from 10-20 WT or DKO (2- to 3-week-old) mice per sample.
2013-12-30 | E-GEOD-31042 | biostudies-arrayexpress
Project description:We investigate the cellular and molecular mechanisms of tumor suppression by NR4A1 and NR4A3, and show a cell intrinsic essential function in maintenance of hematopoietic stem cell (HSC) homeostasis. In the absence of Nr4a1/3, HSC lost quiescence, became highly proliferative leukemia-stem cell (LSC) that transplanted AML to recipient mice. We further revealed that loss of NR4A1/3 leads to deregulated expression of the key cell cycle regulator Cdkn1c (P57), c-Myc oncogene, and glucose metabolic genes leading to enhanced aerobic glycolysis or ‘Warburg effect’ in LSCs. Reintroduction of Nr4a1 in LSCs restored HSC quiescence, and reversed Nr4a1/3 deficiency induced P57 suppression and c-Myc overexpression. Collectively, we identify an essential role of Nr4a1/3 in coordinately regulating cell cycle entry and glucose metabolism to prevent uncontrolled stem cell proliferation and AML transformation. These results have major implications for designing therapeutic strategies in AML.
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Project description:AZIN2 regulates adipocyte progenitor differentiation. Here we investigated how AZIN2 deficiency affects the profile of adipocyte progenitors. To this end, Azin2-/- and wild-type male mice were fed for 8 weeks a high-fat diet, subcutaneous adipose tissue was isolated and single-cell RNA-seq was performed in CD45-CD31- cells of the stromal vascular fraction.
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Project description:White adipose tissue regulates metabolism; the importance of this control is highlighted by the ongoing pandemic of obesity and associated complications such as diabetes, atherosclerosis, and cancer. White adipose tissue maintenance is a dynamic process, very little is known about how pharmacologic stimuli affect such plasticity. Combining in vivo lineage marking and BrdU labeling strategies, we found that rosiglitazone, a member of the thiazolidinedione class of glucose-lowering medicines, markedly increases the evolution of adipose progenitors into adipocytes. Notably, chronic rosiglitazone administration disrupts the adipogenic and self-renewal capacities of the stem cell compartment and alters its molecular characteristics. These data unravel unknown aspects of adipose dynamics and provide a basis to manipulate the adipose lineage for therapeutic ends. The goal of this gene expression array was to identify changes in molecular expression in adipose progenitors isolated from mice that underwent two-month rosiglitazone treatment. Adipose SV GFP+ cells (adipose progenitors) were FACS-isolated from adult AdipoTrak mice that had been treated with or without rosiglitazone (0.0075%) for 2 months. RNAs isolated from these cells were used for microarray. Each cohort contains 3-4 mice, each experimental group (-TZD and +TZD) contains 3 cohorts.
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Project description:Chromatin accessibility analysis of adipose progenitors (AP).
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Project description:White adipose tissue regulates metabolism; the importance of this control is highlighted by the ongoing pandemic of obesity and associated complications such as diabetes, atherosclerosis, and cancer. White adipose tissue maintenance is a dynamic process, very little is known about how pharmacologic stimuli affect such plasticity. Combining in vivo lineage marking and BrdU labeling strategies, we found that rosiglitazone, a member of the thiazolidinedione class of glucose-lowering medicines, markedly increases the evolution of adipose progenitors into adipocytes. Notably, chronic rosiglitazone administration disrupts the adipogenic and self-renewal capacities of the stem cell compartment and alters its molecular characteristics. These data unravel unknown aspects of adipose dynamics and provide a basis to manipulate the adipose lineage for therapeutic ends. The goal of this gene expression array was to identify changes in molecular expression in adipose progenitors isolated from mice that underwent two-month rosiglitazone treatment.
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