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The redox-sensitive transcription factor, Nrf2, regulates murine hematopoietic stem cell survival

ABSTRACT: To better understand the differentiation and survival defect of Nrf2-/- HSPC, we performed gene expression studies on KSL cells isolated by FACS from Nrf2+/+ and Nrf2-/- mice. Gene expression data suggests that loss of Nrf2 leads to global defects in cytokine signaling, and the administration of the exogenous granulocyte colony-stimulating factor (G-CSF) improved HSPC survival despite increasing intracellular ROS.

ORGANISM(S): Mus musculus

PROVIDER: GSE33139 | GEO | 2011/10/22

SECONDARY ACCESSION(S): PRJNA149385

REPOSITORIES: GEO

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The redox-sensitive transcription factor, Nrf2, regulates murine hematopoietic stem cell survival

Project description:To better understand the differentiation and survival defect of Nrf2-/- HSPC, we performed gene expression studies on KSL cells isolated by FACS from Nrf2+/+ and Nrf2-/- mice. Gene expression data suggests that loss of Nrf2 leads to global defects in cytokine signaling, and the administration of the exogenous granulocyte colony-stimulating factor (G-CSF) improved HSPC survival despite increasing intracellular ROS. Bone marrow cells from young healthy Nrf2+/+ and Nrf2-/- mice (n=5 per genotype ) were pooled, stained with KSL cell marker and FACS. Total RNA was isolated from the pooled KSL cells, quantified, amplified and profiled. One pooled RNA sample from each genotype (Nrf2+/+ and Nrf2-/-) was profiled using Affymetrix GeneChip Mouse Gene ST 1.0 chips.

2011-10-21 | E-GEOD-33139 | biostudies-arrayexpress

G-CSFR expression is not essential for neutrophil differentiation but for progenitor formation and emergency neutrophil responses

Project description:Severe congenital neutropenia (SCN) is a rare disorder characterized by a maturation arrest of myeloid progenitor cells in the bone marrow and severe reduction in the amount of circulating neutrophils. Loss-of-function mutations in the CSF3R (the gene encoding the granulocyte colony-stimulating factor (G-CSF) receptor) have been reported in a handful of cases. We describe two novel pedigrees with moderate neutropenia. G-CSFR immunostaining was greatly reduced on patient neutrophils. G-CSF did not prolong neutrophil survival or enhanced reactive oxygen species generation, and STAT-3 phosphorylation was absent, while neutrophils did respond to granulocyte-macrophage colony-stimulating factor (GM-CSF). Despite a lack of G-CSF signaling, morphology and cellular proteomics were normal. We suggest the major role of G-CSF is not in myeloid differentiation, but in generation of sufficient number of committed progenitor cells for neutrophil release and their survival during inflammation, which corresponds with G-CSFR expression in myeloid cell fractions from bone marrow of healthy individuals.

2020-09-25 | PXD018178 | Pride

Transcription profiling time series of mouse bone marrow macrophages treated with macrophage colony stimulating factor or granulocyte colony stimulating factor

Project description:BM monocytes were treated with 20ug/ml of M-CSF (macrophage colony stimulating factor) or GM-CSF (granulocyte monocyte colony stimulating factor) for 0, 6, 12 hours before harvesting RNA for analysis

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Macrophages heterogeneity in human atherosclerotic plaques

Project description:This study aims to characterize the transcriptional profile of Granulocyte-macrophage colony-stimulating factor induced macrophages (GM-MÃ) and M-CSF macrophages (M-MÃ) and to investigate in situ a subset of genes and their products specific to each phenotype in human atherosclerosis plaques 18 RNG/MRC two-colour oligonucleotide microarrays (Le Brigand et al. 2006) were used to generate global mRNA expression profiles for GM-CSF-induced, M-CSF-induced, and peritoneal macrophages. The microarray experiments were conducted either as a common reference (peritoneal-like macrophages) design or using a direct design by hybridizing Granulocyte-macrophage colony-stimulating factor (GM-CSF)-induced human monocyte-derived macrophage (GM-MÃ) and CSF-induced human monocyte-derived macrophages(M-MÃ) on the same arrays

2010-05-16 | E-GEOD-18275 | biostudies-arrayexpress

Hematopoietic stem cells from mice treated with G-CSF or saline alone for 7 days

Project description:Recent studies demonstrate that inflammatory signals regulate hematopoietic stem cells (HSCs). Granulocyte-colony stimulating factor (G-CSF) is often induced with infection and plays a key role in the stress granulopoiesis response. However, its effects on HSCs are less clear. Herein, we show that treatment with G-CSF induces expansion and increased quiescence of phenotypic HSCs, but causes a marked, cell-autonomous HSC repopulating defect associated with induction of toll-like receptor (TLR) expression and signaling. The G-CSF-mediated expansion of HSCs is reduced in mice lacking TLR2, TLR4 or the TLR signaling adaptor MyD88. Induction of HSC quiescence is abrogated in mice lacking MyD88 or in mice treated with antibiotics to suppress intestinal flora. Finally, loss of TLR4 or germ free conditions mitigates the G-CSF-mediated HSC repopulating defect. These data suggest that low level TLR agonist production by commensal flora contributes to the regulation of HSC function and that G-CSF negatively regulates HSCs, in part, by enhancing TLR signaling. RNA from KSL SLAM cells (Lineage- c-Kit+ Sca-1+ CD150+ CD48- CD41-) from bone marrow of 5-10 mice per group treated with G-CSF or saline alone was prepared using the RNA XS column kit (Machery-Nagel), amplified using the NuGen Ovation system (NuGen) and hybridized to the MoGene 1.0 ST array. This array includes 3 independent PBS control and 3 G-CSF treated groups.

2014-02-19 | E-GEOD-55094 | biostudies-arrayexpress

Hematopoietic stem cells from mice treated with G-CSF or saline alone for 36 hours

Project description:Recent studies demonstrate that inflammatory signals regulate hematopoietic stem cells (HSCs). Granulocyte-colony stimulating factor (G-CSF) is often induced with infection and plays a key role in the stress granulopoiesis response. However, its effects on HSCs are less clear. Herein, we show that treatment with G-CSF induces expansion and increased quiescence of phenotypic HSCs, but causes a marked, cell-autonomous HSC repopulating defect associated with induction of toll-like receptor (TLR) expression and signaling. The G-CSF-mediated expansion of HSCs is reduced in mice lacking TLR2, TLR4 or the TLR signaling adaptor MyD88. Induction of HSC quiescence is abrogated in mice lacking MyD88 or in mice treated with antibiotics to suppress intestinal flora. Finally, loss of TLR4 or germ free conditions mitigates the G-CSF-mediated HSC repopulating defect. These data suggest that low level TLR agonist production by commensal flora contributes to the regulation of HSC function and that G-CSF negatively regulates HSCs, in part, by enhancing TLR signaling. RNA from KSL SLAM cells (Lineage- c-Kit+ Sca-1+ CD150+ CD48- CD41-) from bone marrow of 5-10 mice per group treated with G-CSF or saline alone was prepared using the RNA XS column kit (Machery-Nagel), amplified using the NuGen Ovation system (NuGen) and hybridized to the MoGene 1.0 ST array. This array includes 4 independent PBS control and 4 G-CSF treated groups.

2014-02-19 | E-GEOD-55093 | biostudies-arrayexpress

Expression data from persister and normal cells of Pseudomonas aeruginosa PAO1

Project description:Pseudomonas aeruginosa PAO1 persister and normal cells were treated with and without Granulocyte Macrophage Colony-Stimulating Factor (GM-CSF) to understand the effect of GM-CSF on gene expression of PAO1. We used DNA microarrays to identify the down-regulated and up-regulated genes after GM-CSF treatment.

2014-11-25 | GSE63588 | GEO

NRF2 Is Required for Neonatal Beta-Cell Growth by Maintaining Redox Balance and Promoting Mitochondrial Biogenesis and Function

Project description:Due to the limited expression of several antioxidant enzymes, β-cells are highly vulnerable to high ROS levels, which can lead to the reduction of functional β-cell mass. During early postnatal ages, both human and rodent β-cells go through a burst of proliferation that quickly declines with age. Here we discovered that the expression of the master antioxidant regulator, Nrf2, is increased during this postnatal burst of β-cell proliferation in humans. Additionally, data from β-cell specific Nrf2 deletion in mice demonstrated that Nrf2 is required for β-cell proliferation, β-cell survival, β-cell identity and β-cell mass expansion at early stages of life. Daily administration of antioxidant NAC to newborn mice showed that Nrf2 mechanism of action strongly relies on maintaining normal redox balance. Interestingly, RNAseq of islets isolated from β-cell specific Nrf2 deleted mice suggests that Nrf2 regulates neonatal β-cell proliferation by promoting mitochondrial ATP synthesis. Our study highlights Nrf2 as an essential transcription factor for maintaining redox balance as well as mitochondrial biogenesis and function to support neonatal β-cell growth and for maintaining functional β-cell mass in adulthood under metabolic stress.

2023-12-19 | GSE242718 | GEO

Nrf2 transcript alterations

Project description:WGS and RNA-seq data for Nrf2 study

| EGAS00001001740 | EGA

Nrf2 suppresses macrophage inflammatory response by blocking proinflammatory cytokine transcription

Project description:Nrf2 (NF-E2-related factor-2) transcription factor regulates oxidative/xenobiotic stress response and also represses inflammation. However, the mechanisms how Nrf2 alleviates inflammation are still unclear. Here, we demonstrate that Nrf2 interferes with lipopolysaccharide-induced transcriptional upregulation of proinflammatory cytokines, including IL-6 and IL-1Î². ChIP-seq and ChIP-qPCR analyses revealed that Nrf2 binds to the proximity of these genes in macrophages and inhibits RNA Pol II recruitment. Further, we found that Nrf2-mediated inhibition is independent of the Nrf2 binding motif and reactive oxygen species level. Murine inflammatory models further demonstrated that Nrf2 interferes with IL6 induction and inflammatory phenotypes in vivo. Thus, contrary to the widely accepted view that Nrf2 suppresses inflammation through redox control, we demonstrate here that Nrf2 opposes transcriptional upregulation of proinflammatory cytokine genes. This study identifies Nrf2 as the upstream regulator of cytokine production and establishes a molecular basis for an Nrf2-mediated anti-inflammation approach. Gene expression in BMDMs obtained from wild-type and Keap1-CKO mice. In Keap1-CKO (Keap1 flox/flox::LysM-Cre) BMDMs, Nrf2 transcription factor is activated due to Keap1-deficiency. BMDMs were obtained by a culture of bone marrow cells in the presence of M-CSF for7 days. M1-activated BMDMs were obtained by stimulation with LPS and IFNg for 6 hours, while M2-activated BMDMs were obtained by a stimulation with IL-4 for 6 hours. Two independent BMDM cultures were performed, and each experiment contains samples obtained from one wild-type and one Keap1-CKO mice, respectively.

2016-05-12 | E-GEOD-71263 | biostudies-arrayexpress

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