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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. 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.

ORGANISM(S): Mus musculus

SUBMITTER: Biswal Shyam

PROVIDER: E-GEOD-33139 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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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.

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

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Hepatic gene expression profiles after long-term high-fat diet feeding in wild type and Nrf2 knock-out mice.

Project description:To assess the role of the transcription factor NFE2 related factor 2 like 2 ( Nrf2) in the development of high-fat diet (HFD)-induced obesity and non-alcoholic HFD-induced fatty liver disease, 8 wild type (WT) and 8 Nrf2 knock-out (Nrf2-KO) C57BL6J male mice (obtained from Riken BRC, Tsukuba, Japan and originally developed by Prof. M. Yamamoto) were fed an HFD (60 kcal % fat) for 180 days. Whole genome microarray expression profiling was performed in pooled liver samples of WT and Nrf2-KO mice to identify genes that are differentially expressed between WT and Nrf2-KO mice under the stress conditions of HFD-induced obesity. Liver samples were taken from 8 wild type (WT) and 8 Nrf2 knock-out (Nrf2-KO) male mice on high-fat diet (60 kcal % fat) for 180 days. Total RNA was isolated from pooled liver samples from WT or Nrf2-KO mice to produce 4 samples each using the guanidinium thiocyanate method.

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Functional analysis of the cytoprotective transcription factor Nrf2 in keratinocytes: Identification of Nrf2-regulated miRNAs

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Effects of Oltipraz on Gene Expression in the Livers of Wild-Type and Nrf2-null Mice

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Nrf2 bindng in C2C12 myotubes

Project description:Nrf2 (NF-E2-related-factor-2) contributes to the maintenance of glucose homeostasis in vivo. Nrf2 suppresses blood glucose levels by protecting pancreatic Î²-cells from oxidative stress and improving peripheral tissue glucose utilization. To elucidate the molecular mechanisms by which Nrf2 contributes to the maintenance of glucose homeostasis, we generated skeletal muscle (SkM)-specific Keap1-knockout (Keap1MuKO) mice that express abundant Nrf2 in SkM and then examined Nrf2-target gene expression in this tissue. In Keap1MuKO mice, blood glucose levels were significantly downregulated, and the levels of glycogen branching enzyme (Gbe1) mRNA, along with those of glycogen branching enzyme (GBE) protein, were significantly upregulated in mouse SkM. Consistent with this result, chemical Nrf2-inducers promoted Gbe1 mRNA expression in both mouse SkM and C2C12 myotubes. Chromatin-immunoprecipitation analysis demonstrated that Nrf2 binds the Gbe1 upstream promoter regions. In Keap1MuKO mice, muscle glycogen content was strongly reduced, and forced GBE expression in C2C12 myotubes promoted glucose uptake. Therefore, our results demonstrate that Nrf2-induction in SkM increases GBE expression and reduces muscle glycogen content, resulting in improved glucose tolerance. Chromatin occupancy of Nrf2 under CDDO-Im-treated condition were generated by deep sequencing, in dupliplicate

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Hepatic gene expression profiles after long-term high-fat diet feeding in wild type and Nrf2 knock-out mice.

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Identification of Novel NRF2-Regulated Genes by ChIPSeq

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