MC903 / Calcipotriol mouse model treated with GLPG2534 or dexamethasone
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
SUBMITTER:
PROVIDER: E-MTAB-10015 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:miR-146a acts as a negative feedback regulator of inflammation. To investigate the role of miR-146a in psoriasis psoriasiform skin inflammation was indeuced in Mir-146a-/- and wild type mice (C57BL6J) by topical applciation of imiquimod (IMQ)-cream (Aldara). Gene expression profiling (Affymetrix) was used to identify transcriptomic changes associated with psoriasis-like skin inflammation in wild type vs. miR-146a -/-mice. A daily topical dose of 31.25 mg of Aldara cream (5% IMQ) was applied on the right ear of miR-146a -/- and C57BL/6 mice on three consecutive days to induce psorisis-like skin inflammation. Mice were sacrificed at day 4. Ear flaps were collected for total RNA extraction and hybridization on Affymatrix GeneTitan plate format Gene ST 2.1 (mouse).
2016-02-19 | E-GEOD-78057 | biostudies-arrayexpress
Project description:Identification of chemical allergen inducible genes in mouse skin. Ear samples were isolated from CL57BL/6 mice 6 hours after topical application of a prototypic chemical allergen, a skin irritant or vehicle alone. Total RNA were extracted from ear skin samples treated with a chemical allergen, a skin irritant, or vehicle alone for 6 hours.
2011-03-10 | E-GEOD-20726 | biostudies-arrayexpress
Project description:Activation of oncogenes often leads to induction of the DNA damage responses and onset of the cell senescence. Given that DNA damage can also trigger production of type I interferons (IFN) that contribute to senescence development, we sought to determine the role of IFN in the oncogene-induced senescence. Our data in mouse model demonstrate that inactivation of IFN signaling is sufficient for inducing melanomas in melanocytes harboring mutant Braf. Restoration of IFN signaling in IFN-deficient melanoma cells induces cell senescence and suppresses melanoma progression. In addition, data in human patients that received high dose IFN therapy and in mouse transplanted tumor models strongly suggest the importance of the non-cell-autonomous IFN signaling. Suppression of IFN signaling mediated by the downregulation of IFN receptor IFNAR1 invariably occurs during development of mouse melanoma. Mice harboring the IFNAR1 mutant, which is relatively resistant to downregulation, delay melanoma development, suppress the metastatic disease, and better respond to treatment with BRAF or PD1 inhibitors. These results suggest that IFN signaling is an important tumor suppressive pathway that inhibits melanoma development and progression. Accordingly, the inhibition of IFN pathway via IFNAR1 downregulation plays a key role in melanoma pathogenesis. Conversely, these data also argue for targeting IFNAR1 downregulation to prevent the metastatic disease and improve the efficacy of molecularly targeted and immune-targeted therapies. Two genotypes of mice were examined at 2 to 3 times after tamoxifen adminstration, with 2 replicates for each condition, yielding 8 samples in total.
2016-01-14 | E-GEOD-76842 | biostudies-arrayexpress
Project description:In this experiment, mice from 3 strains A/J, Balb C and C57Bl6 were infected with Trypanosoma Congolense, IL1180 clone, African sleeping sickness, a disease which affects cattle in sub-saharan Africa. These mouse strains were chosen because they are a model for tolerance to infection in cattle, with A/J and Balb B being highly susceptible, and C57Bl6 being somewhat more tolerant to infection. Three tissues Kidney Liver and Spleen were harvested from cohorts at various timepoints: 0 (naive), 3, 7, 9 and 17 days post infection. Each condition thus comprises: Time, Tissue, Strain. For each condition, RNA extracts from individuals were pooled (5 per pool) prior to hybridisation.
2007-08-21 | E-MEXP-1190 | biostudies-arrayexpress
Project description:The imiquimod model is used to induce the skin production of IL-22 and to characterize the cells that produce IL-22 in the skin after inflammatory stimulus. This experiment is performed on skin of C57Bl/6 mice treated with imiquimod to induce psoriasis-like lesions. After 5 days of imiquimod treatment, we analysed the heamatopoietic cells that infiltrate the skin and we compared the gene signature of three T cell populations: CD4+ T cells, CD4-CD8-(DN) T cells and gd T cells
2016-08-09 | E-MTAB-4453 | biostudies-arrayexpress
Project description:Transformation of the Arabidopsis ATHB17 gene into maize results in the expression of a truncated protein (smaller by 113 amino acids) that functions as a dominant-negative regulator that can modify activity of endogenous maize HD-Zip II transcription factors. This RNASeq experiment indicates that the observed effects of ATHB17d113 on the maize ear inflorescence and ear transcriptome are very small. Expression of ATHB17delta113 protein in maize leads to changes in ear growth resulting in increased ear size at early reproductive stages and, potentially increased sink size. Two ATHB17delta113 expressing events (Event 1 and Event 2) were compared to control plants (herein referred to as WT) in the context of Monsanto Elite Maize hybrid line NN6306. Three bioreps of both Ear inflorescence and Ear tissues were sampled for the WT and each of the two transgenic events.
2015-10-26 | E-GEOD-51742 | biostudies-arrayexpress
Project description:Children are considered more sensitive to radiation-induced cancer than adults, yet any differences in genomic alterations associated with age at exposure and their underlying mechanisms remain unclear. We analyzed the mutation of key tumor suppressor genes in T-cell lymphomas arising after weekly irradiation of female B6C3F1 mice with 1.2 Gy X-rays for 4 consecutive weeks starting during infancy (1 week old), adolescence (4 weeks old) or as young adults (8 weeks old). T-cell lymphoma incidence did not show any statistical differences among three irradiated groups; however, the frequency of loss of heterozygosity on chromosomes 11 and 19 showed opposing correlations with age at exposure. Ikaros on chromosome 11 was mutated frequently in the young adultâ??irradiation group (63%; 5/8), frequently incurring multiple independent hits (including deletions and mutations) or suffering a single hit predicted to result in a dominant negative protein (such as those lacking exon 4, an isoform we have designated Ik11, which lacks two of the four zincâ??finger domains important for DNA binding). Pten on chromosome 19 was mutated more frequently in tumors from infant- (67%; 10/15) compared with young adult-irradiated mice (13%; 1/8, P = 0.041). Despite the presence of homozygous Pten mutations, DNA copy number was unchanged in the infant-irradiation group, suggesting duplication of the mutated allele by chromosome mis-segregation or mitotic recombination. Taken together, our findings demonstrate that while deletions on chromosome 11 affecting the Ikaros locus are a prominent feature of young adult irradiation-induced T-cell lymphoma, tumors arising after infant irradiation suffer a second hit in the Pten gene by chromosome mis-segregation or recombination. This is the first report showing age-at-exposure associated radiation-induced genomic alterations in two key tumor suppressor genes linked to T-cell lymphomagenesis. These data are important for considering the risks associated with childhood exposure to radiation. 38 T-cell lymphomas arising after weekly irradiation of female B6C3F1 mice with 1.2 Gy X-rays for 4 consecutive weeks starting at different ages (Infant: 1 week old (15 tumors), Adolescent: 4 weeks old (13 tumors), Young adult: 8 weeks old (10 tumors)) were analyzed.
2015-11-12 | E-GEOD-63349 | biostudies-arrayexpress
Project description:Development of a suitable mouse model would facilitate the investigation of pathomechanisms underlying human psoriasis and would also assist in development of therapeutic treatments. However, while many psoriasis mouse models have been proposed, no single model recapitulates all features of the human disease, and standardized validation criteria for psoriasis mouse models have not been widely applied. In this study, whole-genome transcriptional profiling is used to compare gene expression patterns manifested by human psoriatic skin lesions with those that occur in five psoriasis mouse models (K5-Tie2, imiquimod, K14-AREG, K5-Stat3C and K5-TGFbeta1). While the cutaneous gene expression profiles associated with each mouse phenotype exhibited statistically significant similarity to the expression profile of psoriasis in humans, each model displayed distinctive sets of similarities and differences in comparison to human psoriasis. For all five models, correspondence to the human disease was strong with respect to genes involved in epidermal development and keratinization. Immune and inflammation-associated gene expression, in contrast, was more variable between models as compared to the human disease. These findings support the value of all five models as research tools, each with identifiable areas of convergence to and divergence from the human disease. Additionally, the approach used in this paper provides an objective and quantitative method for evaluation of proposed mouse models of psoriasis, which can be strategically applied in future studies to score strengths of mouse phenotypes relative to specific aspects of human psoriasis. Global transcriptional profiling was utilized to evaluate the similarity between human psoriasis and the psoriasis-like phenotypes that develop in five mouse models (K5-Tie2, IMQ, K14-AREG, K5-Stat3C, K5-TGFbeta1) Expression patterns associated with mouse phenotypes were evaluated by comparing lesional skin from transgenic or IMQ-treated mice (n = 2-3) with normal skin obtained from control mice (n = 2-3).
2011-03-03 | E-GEOD-27628 | biostudies-arrayexpress
Project description:To determine the modulation of gene expression of Leishmania mexicana(M379)-inoculated BALB/c ears in the presence of promastigote secretory gel (PSG) A genome-wide transcriptional analysis was performed by comparing the gene expression profiles of Leishmania mexicana- inoculated BALB/c ears and Leishmania mexicana plus PSG BALB/c ears. Leishmania mexicana amastigotes were purified from mouse cutaneous lesions and transformed in vitro in metacycic promastigotes (MT). After 6, 24 and 48 hours, ears were collected and processed for RNA extraction. Three Biological replicates per condition were run.
2013-12-17 | E-GEOD-52101 | biostudies-arrayexpress
Project description:This dataset contains three experiments, designed for interrogating the effect of DETC on epithelial keratinocytes: Dataset 1) steady state ear epithelial cells (live, CD45-) from C57BL6/N (n=3) and Tcrd-GDL (n=3), after DETC deletion. Dataset 2) untreated and topical TPA-treated ear epithelial cells (live, CD45-, Vg5-) from C57BL6/J (n=3 untreated ears, n=3 treated ears). Dataset 3) steady state ear epithelial cells (GFP+) from CD1 (n=6) mice at age p8 weeks, following transduction with IL13Ra1-shRNA-GFP at e9.5.
2022-12-31 | E-MTAB-10441 | biostudies-arrayexpress