Gene expression in mice brain after ciguatoxin exposure
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
SUBMITTER: Jimmy Ryan
PROVIDER: E-GEOD-20949 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:Ciguatoxins (CTX) are polyether neurotoxins responsible for ciguatera, the most common fish-borne food poisoning in humans. This study characterizes the global transcriptional response of mouse liver to a symptomatic dose (0.26 ng/g) of the highly potent Pacific ciguatoxin-1 (P-CTX-1). At 1 h post exposure 2.4% of features on a 44K whole genome array were differentially expressed (p � 0.0001), increasing to 5.2% at 4 h and decreasing to 1.4% by 24 h post-CTX exposure. Early gene expression was likely influenced prominently by an acute 4 °C decline in core body temperature by 1 h, which resolved by 8 h following exposure. Cytochrome P450s were of particular interest due to their role in xenobiotic metabolism. Twenty-seven genes, mostly members of Cyp2 and Cyp4 families, showed significant changes in expression. Many Cyps underwent an initial down-regulation at 1 h but were quickly and strongly up-regulated at 4 and 24 h post exposure. In addition to Cyps, increases in several glutathione S-transferases were observed, an indication that both phase I and phase II metabolic reactions are involved in the hepatic response to CTX in mice. Experiment Overall Design: Individual C57/BL6 mice (n=3) exposed to 0.26 ng/g P-CTX-1 ip for 1, 4, or 24 h were compared to pooled time-matched controls (n=3). The triplicate arrays at each time point included a dye swap.
2008-06-20 | E-GEOD-10768 | biostudies-arrayexpress
Project description:This experiment describes gene expression after the activation of APETALA1-GR, to study and identify AP1 target genes. We used a 35S:AP1-GR ap1 cal line to induce a synchronized response activating the AP1-GR fusion protein in ap1 cal inflorescence-like meristems through dexamethasone or dexamethasone+cycloheximide treatment. Tissue samples were collected at 3hrs after the treatment. The expression profiles of the individual samples were then analyzed by gene expression profiling using whole-genome oligonucleotide arrays (Agilent, custom-commercial). We treated inflorescences of 35S:AP1-GR ap1-1 cal-1 plants with a dexamethasone-containing or a mock solution, or with identical solutions that contained in addition 10 M-NM-<M cycloheximide. Tissue was collected 3 hours after the treatment. Samples from each of the four biological replicates resulted in a set of four hybridization pairs: Mock vs. Dex, Mock vs. Chx, Mock vs. Dex+Chx, and Chx vs. Dex+Chx. Dye polarities were switched between biological replicates.
2011-01-01 | E-GEOD-20175 | biostudies-arrayexpress
Project description:The molecular mechanisms that control innate cell recruitment during chronic infection and inflammation, such as tuberculosis (TB), are incompletely understood. During TB, myeloid cells infiltrate the lung and sustain local inflammation. We identified microRNA (miR)-223 as one of the most abundant noncoding RNAs in lung parenchyma of TB patients and susceptible mice. MiR-223 controlled lung recruitment of myeloid cells, and consequently, neutrophil-driven lethal inflammation, by directly targeting the chemoattractants CXCL2, CCL3 and IL-6. Our study reveals an essential role for a single miR in TB. Moreover, we identify new targets for and assign novel biological functions to miR-223. By regulating leukocyte chemotaxis via chemoattractants, miR223 is critical for control of TB and probably other nonresolving inflammatory diseases. MicroRNAs expression analysis in whole blood from 8 TB and 8 TST+ subjects. The samples were collected at Makerere University in Kampala, Uganda. Gene expression analysis of whole blood and lung tissue of C57/BL6 and miR-223-/- mouse strains (8-12 weeks of age) after Mtb aerosol infection. Samples were collected at 7, 14 and 21 days post infection.
2014-04-21 | E-GEOD-39163 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the following subset Series: GSE20139: Ath_Agilent_v1_Riechmann array expression profile AP1-GR ap1cal inflorescences - time series (hours) GSE20182: Meyerowitz Lab Arabidopsis Operon Array v4 - 4200A scanner - AP1-GR ap1cal inflorescences - time series (hours) GSE20183: Meyerowitz Lab Arabidopsis Operon Array v4 - 4000B scanner - AP1-GR ap1cal inflorescences - time series (hours) Refer to individual Series
2010-04-02 | E-GEOD-20184 | biostudies-arrayexpress
Project description:Ataxia telangiectasia (AT) is an autosomal recessive disorder characterized by neuronal degeneration, telangiectasias, acute cancer predisposition, and hypersensitivity to ionizing radiation (IR). The gene defective in AT, ATM (for AT-mutated), encodes a protein, pATM that has been found to have IR-inducible kinase activity. Cells from individuals with AT exhibit severely attenuated cell cycle checkpoints in response to gamma radiation exposure. pATM has been hypothesized to act as part of a complex that senses DNA damage, in particular, DNA double strand breaks. We are studying the pATM-dependent gene expression responses to a dose of 1.5 Gy radiation in lymphoblastoid cell lines from multiple individuals with either wild type or mutated ATM. The gene expression analyses were performed on Agilent Human 1A Oligo chips containing approximately 16,000 60mer probes. We identified a set of genes whose gene expression changes are ATM-dependent following exposure to 1.5 Gy IR. This set of genes was tested by real time quantitative PCR analysis. The study consists of one dose group - 1.5 Gray gamma radiation. Samples were collected 6 hr following irradiation (treated) or mock irradiation (controls) for each culture. Each culture has a treated sample and a control sample. There are cultures from 6 wild-type ATM individuals and cultures from 6 individuals that are ATM-deficient, for a total of 12 cultures. Hybridizations compared RNA extracted from each individual culture's treated sample against its corresponding control sample, and were performed as dye-flip duplicates (1 replicate in each direction). Hybridizations were performed on the Human 1A Oligo Chips using low input, direct labeling at Paradigm Genetics Laboratory. Microarray scanning was performed with the Agilent G2565AA Scanner. Paradigm Standard Operating Procedures were followed for quality analysis, sample labeling, microarray hybridization and washing, scanning, image analysis and initial data analysis.
2013-12-02 | E-GEOD-19287 | biostudies-arrayexpress
Project description:This experiment describes gene expression after the activation of APETALA1-GR, to study and identify AP1 target genes. We used a 35S:AP1-GR ap1 cal line to induce a synchronized response activating the AP1-GR fusion protein in ap1 cal inflorescence-like meristems through dexamethasone treatment. Tissue samples were collected immediately after the treatment, as well as subsequent timepoints. The expression profiles of the individual samples were then analyzed by gene expression profiling using whole-genome oligonucleotide arrays (Agilent, custom-commercial). Keywords: time course Four sets of biologically independent tissue samples were collected at 0, 2, 4, 8, and 12 hours after the application of dexamethasone (Dex-; activation of the AP1-GR fusion protein) or a mock solution (Mock-; control). Dex- and Mock-derived samples for each timepoint and biological replicate were co-hybridized; one sample was labeled with Cy3 and the other with Cy5. The dyes used for labeling RNA from a given treatment type (Dex and Mock, at a given timepoint) were switched for two of the replicate experiments, to reduce dye-related artifacts. This experimental setup resulted in a total of 5 hybridizations per set (0h, 2h, 4, 8h, and 12h; Dex vs. Mock at each timepoint), and an even number (2) of hybridizations of each dye polarity per timepoint. The combined ratio data results are available as a supplementary file on the Series record.
2010-04-02 | E-GEOD-20139 | biostudies-arrayexpress
Project description:Comparion of gene expression profiles of wild-type and apetala1 inflorescences The gene expression profile of inflorescences of the floral homeotic mutant apetala1 was compared to wild-type inflorescences (Ler) using a whole-genome oligonucleotide array (Agilent, custom-commercial). Experiment was performed in triplicate. This series contains the data for three replicate experiments performed with three sets of independent samples. The combined ratio data results are available as a supplementary file on the Series record.
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2014-02-09 | E-GEOD-54722 | biostudies-arrayexpress
Project description:Intracellular parasites reprogram the host functions for their survival and reproduction. Conversely, the infected host attempts to defend the microbial insult. The extent and relevance of parasite-mediated host response in vivo remains poorly studied. We utilized Eimeria falciformis, an obligate intracellular parasite completing its entire life cycle in the mouse intestinal epithelium, to identify and validate the host determinants of the parasite infection. The most prominent mouse genes induced during the onset of asexual (24 hrs) and sexual (144 hrs) parasite cycle include IFNg-regulated factors, e.g., immunity-related GTPases IRGA6/B6/D/M2/M3, guanylate-binding proteins GBP2/3/5/8, chemokines CxCL9-11 and several enzymes of the kynurenine pathway including indoleamine 2,3-dioxygenase 1 (IDO1). These results indicated a multifarious innate defense (tryptophan catabolism, IRG, GBP, chemokines signaling) mounted by epithelial cells, and a consequential adaptive immune response (chemokines-cytokines signaling, lymphocyte recruitment). A notable increase in the inflammation- and immunity-associated transcripts correlated with the severity of infection and influx of B-cells, T-cells and macrophages to the parasitized tissue. Indeed, parasite growth was enhanced in the animals inhibited for CxCr3, a major chemokine receptor on immune cells. Interestingly, despite a prominent induction, the mouse IRGB6 failed to recognize and disrupt the parasitophorous vacuole in the parasite cultures, implying an immune evasion by E. falciformis. Likewise, the oocyst output was impaired in IFNg-R-/- and IDO1-/- mice, which signifies a subversion of IFNg-signaling by the parasite to promote its growth. In brief, the Eimeria-rodent model shows contrasting roles of IFNg-signaling for parasite development, identifies a retinue of potential host determinants, and epitomizes its efficacy for in vivo parasite-host interaction studies. Microarray experiments were performed as dual-color hybridizations on Agilent mouse whole genome catalog 44K arrays. To compensate for dye-specific effects, a dye-reversal color-swap was applied.
2014-01-01 | E-GEOD-49948 | biostudies-arrayexpress
Project description:Background: Stathmin (STMN1) protein functions to regulate assembly of the microtubule cytoskeleton by destabilizing microtubule polymers. Stathmin over-expression has been correlated with cancer stage progression, while stathmin depletion leads to death of some cancer cell lines in culture. In contrast, stathmin-null mice are viable with minor axonopathies and loss of innate fear response. Several stathmin binding partners, in addition to tubulin, have been shown to affect cell motility in culture. To expand our understanding of stathmin function in normal cells, we compared gene expression profiles, measured by microarray and qRT-PCR, of mouse embryo fibroblasts isolated from STMN1+/+ and STMN1-/- mice to determine the transcriptome level changes present in the genetic knock-out of stathmin. Results: Microarray analysis of STMN1 loss at a fold change threshold of 2.0 revealed expression changes for 437 genes, of which 269 were up-regulated and 168 were down-regulated. Microarray data and qRT-PCR analysis of mRNA expression demonstrated changes in the message levels for STMN4, encoding RB3, a protein related to stathmin, and in alterations to many tubulin isotype mRNAs. KEGG Pathway analysis of the microarray data indicated changes to cell motility-related genes, and qRT-PCR plates specific for focal adhesion and ECM proteins generally confirmed the microarray data. Several microtubule assembly regulators and motors were also differentially regulated in STMN1-/- cells, but these changes should not compensate for loss of stathmin. Conclusions: Approximately 50% of genes up or down regulated (at a fold change of ≥ 2) in STMN1-/- mouse embryo fibroblasts function broadly in cell adhesion and motility. These results support models indicating a role for stathmin in regulating cell locomotion, but also suggest that this functional activity may involve changes to the cohort of proteins expressed in the cell, rather than as a direct consequence of stathmin-dependent regulation of the microtubule cytoskeleton. Gene expression of mouse embryo fibroblasts lacking stathmin reveal changes in genes contributing to cell motility Two-color Agilent 4x44k chips with dye-swap on 2 of 4 arrays. Replicate data presented.
2009-07-31 | E-GEOD-17432 | biostudies-arrayexpress