Project description:We found that AhR, a unique chemical sensor, is critical in controlling mast cell differentiation, growth and function in vitro and in vivo. This study seeks to further the understanding of the mechanisms of how AhR control mast cell homeostasis. Three different batches of bone marrow derived mast cells (BMMCs) from AhR null, AhR_d and normal control mice were cultured in 30% WEHI-3-conditioned medium. BMMCs were purified by negative selection with MicroBeads (Miltenyi Biotec) after 4 weeks in culture. 99% BMMCs were FcM-NM-5RI+ c-kit+ CD49b- by flow cytometry analysis. The cells were further rested in cytokine free medium for 4h. Subsequently, total RNA was collected. Gene expression profiling was performed on total RNA from mast cells using Illumina SentrixM-BM-. Murine Ref8_v2_R3 BeadChips. Details of the design and the gene signatures found are given in the paper associated with this GEO Series: Yufeng Zhou, Hui-Ying Tung, Ying-Ming Tsai, Shih-Chang Hsu, Hui-Wen Chang, Hirokazu Kawasaki, Hsiao-Chun Tseng, Beverly Plunkett, Peisong Gao, Chih-Hsin Hung, Becky M. Vonakis, and Shau-Ku Huang. M-bM-^@M-^\Aryl hydrocarbon receptor controls murine mast cell homeostasisM-bM-^@M-^], Blood 2013 Mar 5 [Epub ahead of print]
Project description:[original Title] Comparison of expression data of primary murine melanocytes from aryl hydrocarbon deficient mice and corresponding wild-type C57BL/6 mice Melanin is produced exclusively by melanocytes and melanogenesis is the vital response to protect skin cells against Ultraviolet B (UVB)-induced DNA damage. The aryl hydrocarbon receptor (AhR) is a transcription factor, which may be involved in the physiological tanning response. Normal murine melanocytes express functional AhR. We tested gene expression in WT versus AhR-deficient mice primary murine melanocytes, isolated from the skin and cultivated for several passages. Skin epidermal cells from 2 individual C57BL/6 mice and 2 individual AhR-deficient mice (deletion of exon2, AhRtm1Bra) were grown for 6-8 weeks in selection medium to propagate melanocytes.
Project description:[original Title] Comparison of expression data of primary murine melanocytes from aryl hydrocarbon deficient mice and corresponding wild-type C57BL/6 mice Melanin is produced exclusively by melanocytes and melanogenesis is the vital response to protect skin cells against Ultraviolet B (UVB)-induced DNA damage. The aryl hydrocarbon receptor (AhR) is a transcription factor, which may be involved in the physiological tanning response. Normal murine melanocytes express functional AhR. We tested gene expression in WT versus AhR-deficient mice primary murine melanocytes, isolated from the skin and cultivated for several passages.
Project description:We have generated transgenic mice expressing constitutively activated aryl hydrocarbon receptor (CA-AhR) to examine the biological consequences of AhR activation.. We used microarrays to identify genes that are regulated by AhR.
Project description:We report sequencing of chromatin immunoprecipitated DNA (ChIP-Seq) of Aryl Hydrocarbon Receptor (AHR) targets from decidual stromal cells with kynurenine treatment and normal decidualization media
Project description:We have generated transgenic mice expressing constitutively activated aryl hydrocarbon receptor (CA-AhR) to examine the biological consequences of AhR activation.. We used microarrays to identify genes that are regulated by AhR. Livers or intestines from three female mice were pooled at 5-6 week-old for RNA extraction and hybridization on Affymetrix Mouse Genome 430 2.0 Array.
Project description:To investigate the RNA differences in skeletal muscle in muscle-specific AHR (aryl hydrocarbon receptor) knockout mice and their AHR-floxed littermate controls (wildtype) following a 16-week chronic cigarette smoke exposure intervention
Project description:To identify aryl hydrocarbon receptor (AHR) dependent transcriptional changes in mouse colon stem cells, we performed RNA sequencing of colon organoids from wildtype and AhR deficient mice stimulated with an high affinity AHR ligand, 5nM FICZ for 4 hours.
Project description:Emerging studies revealed an immunomodulatory role of the Aryl hydrocarbon receptor (AhR), a receptor sensing environmental contaminants, and involved in their detoxification. Besides its function as a transcription factor, AhR can participate in non-genomic signaling through ubiquitination and phosphorylation-dependent processes. In this study, a multi-PTM-omics approach, including proteome, ubiquitome, and phosphoproteome, was utilized to examine mechanisms of non-genomic AhR-signaling in endotoxin-activated monocyte-derived macrophages. This dataset entails proteome and phosphoproteome data.
Project description:Conventional biochemical and molecular techniques identified previously several genes whose expression is regulated by the aryl hydrocarbon receptor (AHR). We sought to map the complete spectrum of AHR-dependent genes in male adult liver using expression arrays to contrast mRNA profiles in Ahr-null mice (Ahrâ/â) with those in mice with wild-type AHR (Ahr+/+). Transcript profiles were determined both in untreated mice and in mice treated 19 h earlier with 1000 µg/kg 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Expression of 456 ProbeSets was significantly altered by TCDD in an AHR-dependent manner, including members of the classic AHRE-I gene battery, such as Cyp1a1, Cyp1a2, Cyp1b1, and Nqo1. In the absence of exogenous ligand, AHR status alone affected expression of 392 ProbeSets, suggesting that the AHR has multiple functions in normal physiology. In Ahrâ/â mice, only 32 ProbeSets exhibited responses to TCDD, indicating that the AHR is required for virtually all transcriptional responses to dioxin exposure in liver. The flavin-containing monooxygenases, Fmo2 and Fmo3, considered previously to be uninducible, were highly induced by TCDD in an AHR-dependent manner. The estrogen receptor alpha as well as two estrogen-receptor-related genes (alpha and gamma) exhibit AHR-dependent expression, thereby extending cross-talk opportunities between the intensively studied AHR and estrogen receptor pathways. p53 binding sites are over-represented in genes down-regulated by TCDD, suggesting that TCDD inhibits p53 transcriptional activity. Overall, our study identifies a wide range of genes that depend on the AHR, either for constitutive expression or for response to TCDD. Experiment Overall Design: Mice bearing wild-type or genetically deleted AHRs were treated with corn oil vehicle or TCDD, and their livers analyzed by expression arrays.
