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Gene induction by Dex, IL-9 and CCL-1 in BW5147 mouse T cell lymphoma

ABSTRACT: The aim of this work was to determine the genes and mechanisms involved in IL-9- and CCL1-mediated protection against glucocorticoid-induced apoptosis. We made the hypothesis that the expression of the really critical mediators could be regulated in a reciprocal way by Dex on the one hand and anti-apoptotic cytokines such as IL-9 and CCL1 on the other hand.Therefore, we performed a comprehensive study of the genes expressed by BW5147 cells stimulated with or without Dex, IL-9 and CCL1, taking advantage of the Affymetrix microarray technology. Keywords: cytokine and dexamethasone stimulation

ORGANISM(S): Mus musculus

PROVIDER: GSE13823 | GEO | 2011/05/25

SECONDARY ACCESSION(S): PRJNA110493

REPOSITORIES: GEO

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Gene induction by Dex, IL-9 and CCL-1 in BW5147 mouse T cell lymphoma

Project description:The aim of this work was to determine the genes and mechanisms involved in IL-9- and CCL1-mediated protection against glucocorticoid-induced apoptosis. We made the hypothesis that the expression of the really critical mediators could be regulated in a reciprocal way by Dex on the one hand and anti-apoptotic cytokines such as IL-9 and CCL1 on the other hand.Therefore, we performed a comprehensive study of the genes expressed by BW5147 cells stimulated with or without Dex, IL-9 and CCL1, taking advantage of the Affymetrix microarray technology. Keywords: cytokine and dexamethasone stimulation One million BW5147 cells were stimulated with 100 ng/ml of dexamethasone and/or with 100 U/ml of IL-9 or CCL1 for eight hours. RNA was then extracted for hybridization on Affymetrix microarrays. This experiment was performed in duplicates .

2011-05-25 | E-GEOD-13823 | biostudies-arrayexpress

Intestinal epithelial GR in response to DEX treatment

Project description:The goal of this project is to investigate the role of glucocorticoids and their receptor, glucocorticoid receptor (GR) , in intestinal stress response and tissue homeostasis.We generated a mouse model with specific deletion of GR in intestinal epithelium (GR iKO mice) and examined colonic transcriptomes of adrenalectomized (ADX) Flox control and GR iKO mice in response to dexamethasone (DEX) treatment by microarray analysis.

2021-11-15 | GSE146086 | GEO

Expression data of liver samples of dex or vehicle treated wildtype and HDAC6- knockout C57Bl/6 mice respectively

Project description:In the present study, we investigated the importance of histone deacetylase 6 (HDAC6) for glucocorticoid receptor (GR) mediated effects on glucose metabolism, and its potential as a therapeutic target for the prevention of glucocorticoid (GC)-induced diabetes. Dexamethasone (dex)-induced hepatic glucose output and GR translocation were analysed in wildtype (wt) and HDAC6-deficient (HDAC6ko) mice. The effect of the specific HDAC6-inhibitor tubacin was analysed in-vitro. Wt and HDAC6ko mice were subjected to 3 weeks dex treatment before analysis of glucose and insulin tolerance. HDAC6ko mice showed impaired dex-induced hepatic GR translocation. Accordingly, dex induced expression of a large number of hepatic genes was significantly attenuated in mice lacking HDAC6 and by tubacin in-vitro. Glucose output of primary hepatocytes from HDAC6ko mice was diminished. A significant improvement of dex-induced whole-body glucose intolerance as well as insulin resistance in HDAC6ko mice compared to wt littermates was observed. The present study demonstrates that HDAC6 is an essential regulator of hepatic GC stimulated gluconeogenesis and impairment of whole body glucose metabolism through modification of GR nuclear translocation. Selective pharmacological inhibition of HDAC6 may provide a future therapeutic option against the pro-diabetogenic actions of GCs. In this dataset, we include the expression data obtained from isolated RNA of dissected mouse livers using wildtype and HDAC6 deficient animals which were treated over a timespan of 3 weeks with 1mg/kg dexamethasone and vehicle respectively. These data are used to show the hdac6-deficiency mediated attenuation of several dexamethasone induced genes. 12 samples in total were analyzed. 3 samples of different animals of each group (wt vehicle, wt dexamethasone, hdac6ko vehicle and hdac6ko dexamethasone)

2011-12-07 | E-GEOD-34229 | biostudies-arrayexpress

Expression data of liver samples of dex or vehicle treated wildtype and HDAC6- knockout C57Bl/6 mice respectively

2011-12-07 | GSE34229 | GEO

Jakyak-gamcho-tang ameliorates dexamethasone (DEX)-induced muscle atrophy and muscle dysfunction [Gastrocnemius and Soleus]

Project description:Jakyak-gamcho-tang (JGT) is a herbal medicine that has been traditionally prescrived for pain control including muscular pain. Muscle atrophy is a disease that is characterized with a gradual muscle loss. Muscle atrophy is clearly observed in experimental animals that receive a repeated high-dose of an artificial glucocorticoid, dexamethasone (DEX). This transcriptome analysis aims to investigate the changes in global gene expression profiles in gastrocnemius (GA) and soleus (SO) muscle tissues from mice with DEX-induced muscle atrophy in the presence or absence of JGT co-treatment.

2023-03-21 | GSE227495 | GEO

The autophagy receptor p62/SQSTM1 mediates anti-inflammatory actions of the selective glucocorticoid receptor modulator CpdA in macrophages

Project description:Glucocorticoids are widely used to treat inflammatory disorders. Prolonged use results in side effects including osteoporosis, diabetes and obesity. The selective glucocorticoid receptor (GR) modulator Compound A (CpdA) exhibits an inflammation-suppressive effect, largely in absence of detrimental side effects. To understand the mechanistic differences between the classic glucocorticoid dexamethasone (DEX) and CpdA, we looked for proteins oppositely regulated using an unbiased proteomics approach. We found that the autophagy receptor p62 but not GR mediates the anti-inflammatory action of CpdA in macrophages. CpdA drives the upregulation of p62 by recruiting the NRF2 transcription factor to its promoter. Contrarily, the classic GR ligand dexamethasone recruits GR to p62 and other NRF2 controlled gene promoters, resulting in gene downregulation. Both DEX and CpdA are able to induce autophagy, albeit in a cell-type and time-dependent manner. Suppression of LPS-induced IL-6 and MCP1 genes in bone marrow-derived macrophages by CpdA is hampered upon p62 silencing, confirming that p62 is essential for the anti-inflammatory capacity of CpdA. Together, these results demonstrate how off-target mechanisms of selective GR ligands may establish a more efficient anti-inflammatory therapy

2022-06-03 | PXD007793 | Pride

Expression profiling of shoot apices of 35S::WOX1:GR seedlings transiently treated with DEX

Project description:The WOX1 transcription factor is a multifunctional regulator of lateral-organ development that acts as a transcriptional repressor. WOX1 promotes lamina growth, controls marginal tissue differentiation and is involved in establishment and maintenance of the adaxial-abaxial pattern from the middle domain of leaf primordia. To identify the WOX1 downstream genes, we performed a microarray analysis of shoot apices of transgenic Arabidopsis thaliana lines harboring 35S::WOX1:glucocorticoid receptor (GR) in which the WOX1 function was temporarily enhanced by dexamethasone (DEX).

2018-05-11 | GSE79647 | GEO

Comparison of MPA regulated gene expression profiles to those regulated by PROG, DHT, DEX

Project description:Medroxyprogesterone acetate (MPA) is a progestin that can bind to and activate progesterone, androgen and glucocorticoid receptors. However, it is not known which receptor mediates MPA action in a cellular context where all three of these receptors are co-expressed and functional. This microarray experiment was performed to compare the transcriptomes induced by MPA and the cognate ligands for these receptors ie progesterone (PROG), 5a-dihydrotestosterone (DHT) and dexamethasone (DEX) in breast cancer cells to determine which was most similar to MPA.

2020-01-22 | GSE139870 | GEO

Profiling of Polyadenylated RNAs after Brg1/Smarca4 knock-down in murine bone marrow-derived macrophages after LPS or LPS plus Dex stimulation [RNA-seq]

Project description:We performed Brg1 (Smarac4) knock-down by siRNA in murine primary bone marrow-derived macrophages and profiled the effect on gene expression by RNAseq after lipopolysaccharide (LPS) or LPS plus dexamethasone (Dex) treatment. Brg1 knock-down cells are compared to cells treated with a control siRNA. We analysed the requirement of Brg1/Smarca4 for the expression of inflammatory and glucocorticoid receptor target genes.

2023-10-31 | GSE186513 | GEO

RNA-Seq in LPS and Dex+LPS treated bone marrow-derived macrophages

Project description:Wild-type bone marrow-derived macrophages (BMDMs) were treated with vehicle (0.1% EtOH/D-PBS), 6h 100 ng/ml lipopolysaccharide (LPS) or 16h 1uM dexamethasone (Dex) and 6h 100 ng/ml LPS (Dex+LPS) and mRNA expression analysed by RNA-Seq.

2020-12-31 | GSE137412 | GEO

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