Expression data from diet-induced obesity Oma1-deficient mice.
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
SUBMITTER: Jose Freije
PROVIDER: E-GEOD-27525 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:Adamts12-deficient mice undergo more severe colitis than WT mice after induction with DSS. We used microarrays to determine the gene expression differences between Adamts12-deficient and WT mice during ulcerative colitis induced with DSS (dextran sodium sulfate) Fragments of distal colon from DSS-treated (2% DSS during 7 days and 1 day of recovery) and untreated Adamts12-deficient and WT mice were obtained for RNA extraction and hybridiztion with Affymetrix microarrays
2012-09-01 | E-GEOD-40529 | biostudies-arrayexpress
Project description:Transriptional profiling of white adipose tissue extracted from obese mice.
2012-01-01 | GSE27525 | GEO
Project description:The identification of inflammatory bowel disease (IBD) susceptibility genes by genome-wide association has linked this pathology to autophagy, a lysosomal degradation pathway that is crucial for cell and tissue homeostasis. Here, we describe autophagin-1 (ATG4B) as an essential protein in the control of inflammatory response during experimental colitis. In this pathological condition, ATG4B protein levels increase paralleling the induction of autophagy. Moreover, ATG4B expression is significantly reduced in affected areas of the colon from IBD patients. Consistently, atg4b-/- mice present Paneth cell abnormalities, as well as an increased susceptibility to DSS-induced colitis. Atg4b-deficient mice exhibit significant alterations in proinflammatory cytokines and mediators of the immune response to bacterial infections, which are reminiscent of those found in patients with Crohn’s disease or ulcerative colitis. Additionally, antibiotic treatments and bone marrow transplantation from wild-type mice reduced colitis in atg4b-/- mice. Taken together, these results provide additional evidence on the importance of autophagy in intestinal pathologies and describe ATG4B as a novel protective protein in inflammatory colitis. Finally, we propose that Atg4b-null mice are a suitable model for in vivo studies aimed at testing new therapeutic strategies for intestinal diseases associated with autophagy deficiency Seven samples were collected in total: three from wild-type mice (1 from the ileum and the colon of control mice, and 1 from the colon of a DSS-treated mouse) and four from Atg4b knock-out mice (1 from the ileum and the colon of control mice, and 2 from the colon of DSS-treated mice).
2013-09-16 | E-GEOD-36056 | biostudies-arrayexpress
Project description:Label-free LC-MS/MS was used to characterise and quantify the secretory profiles of murine perivascular adipose tissue, canonical white adipose tissue, and brown adipose tissue.
2022-11-15 | PXD031271 | Pride
Project description:Identification of genes that are differentially regulated in fibroblasts derived from dysplastic oral mucosa and oral squamous cell carcinoma compared to fibroblasts derived from normal oral mucosa. Affymetrix microarrays were used to define differential gene expression. Populations of fibroblasts were isolated from human normal oral mucosa, oral dysplasia and oral squamous cell carcinoma, maintained in 3D collagen I biomatrices, RNA extracted and processed for Affymetrix arrays. Fibroblasts maintained as monolayers were also included as comparators.
2013-12-01 | E-GEOD-38517 | biostudies-arrayexpress
Project description:Transcriptional profiling of human control and Néstor-Guillermo Progeria Syndrome (NGPS) fibroblasts and induced pluripotent stem cells (iPSCs). Somatic cell reprogramming involves rejuvenation of adult cells and relies on the ability to erase age-associated molecular marks. Accordingly, reprogramming efficiency declines with ageing, and age-associated features such as genetic instability, cell senescence or telomere shortening negatively affect this process. However, the regulatory mechanisms that constitute age-associated barriers for cell reprogramming remain largely unknown. Here, by using cells from patients with premature ageing, we demonstrate that NF-κB activation is a critical barrier for the generation of induced pluripotent stem cells (iPSCs) in ageing. We show that NF-κB repression occurs during cell reprogramming towards a pluripotent state. Conversely, ageing-associated NF-κB hyperactivation impairs generation of iPSCs by eliciting reprogramming repressors DOT1L and YY1, reinforcing cell senescence signals and down-regulating pluripotency genes. We also show that genetic and pharmacological NF-κB inhibitory strategies significantly increase the reprogramming efficiency of fibroblasts from Néstor-Guillermo Progeria Syndrome (NGPS) and Hutchinson-Gilford Progeria Syndrome (HGPS) patients, as well as from normal aged donors. Finally, we demonstrate that DOT1L inhibition in vivo ameliorates the accelerated ageing phenotype and extends lifespan in a progeroid animal model. Collectively, our results provide evidence for a novel role of NF-κB in the control of cell fate transitions and reinforce the interest of studying age-associated molecular impairments to implement cell reprogramming methodologies, and to identify new targets of rejuvenation strategies. Control and NGPS fibroblasts were reprogrammed. RNA was extracted and transcriptional profiling was obtained with GeneChip Human Exon 1.0 ST Arrays.
2015-07-01 | E-GEOD-65170 | biostudies-arrayexpress
Project description:Hutchinson-Gilford Progeria Syndrome (HGPS) is caused by a point mutation in the LMNA gene that activates a cryptic donor splice site and yields a truncated form of prelamin A called progerin. Small amounts of progerin are also produced during normal aging. Studies with mouse models of HGPS have allowed the recent development of the first therapeutic approaches for this disease. However, none of these earlier works have addressed the aberrant and pathogenic LMNA splicing observed in HGPS patients because of the lack of an appropriate mouse model. We report herein a genetically modified mouse strain that carries the HGPS mutation. These mice accumulate progerin, present histological and transcriptional alterations characteristic of progeroid models, and phenocopy the main clinical manifestations of human HGPS, including shortened life span and bone and cardiovascular aberrations. By using this animal model, we have developed an antisense morpholino–based therapy that prevents the pathogenic Lmna splicing, dramatically reducing the accumulation of progerin and its associated nuclear defects. Treatment of mutant mice with these morpholinos led to a marked amelioration of their progeroid phenotype and substantially extended their life span, supporting the effectiveness of antisense oligonucleotide–based therapies for treating human diseases of accelerated aging. 6 samples, three from LmnaG609G/G609G mice and three from control Lmna+/+ mice
2012-01-13 | E-GEOD-32609 | biostudies-arrayexpress
Project description:In mammalian cells, AU-rich elements (AREs) are well known regulatory sequences located in the 3' untranslated region (UTR) of many short-lived mRNAs that suppress gene expression at the posttranscriptional level. Tis11, a zinc finger RNA-binding protein homologous to mammalian tristetraprolin, targets ARE-containing reporter mRNAs for rapid degradation in SL2 cells. To identify Drosophila mRNA targets of Tis11, we performed genome-wide expression profiling after dsRNA-mediated depletion of endogenous Tis11 in SL2 cells. Furthermore, we studied the involvement of Tis11 in regulating the Drosophila immune response by profiling mRNA expression after LPS treatment, in the presence or absence of Tis11. SL2 cells were treated with either dsRNA against Tis11 or dsRNA against GFP (control). After 4 days of treatment with 12.5 microgram dsRNA / ml medium, total RNA was extracted and hybridized to Drosophila Genome 2.0 Arrays (Affymetrix, Cat. No. 900531). Where indicated, cells were treated with lipopolysaccharide (LPS, Sigma, O55:B5) at a concentration of 10 microgram / ml for 4 hours before lysis. All experiments were performed in 3 biological replicates.
2011-03-24 | E-GEOD-28147 | biostudies-arrayexpress
Project description:ß-chloroprene (2-chloro-1,3-butadiene), a monomer used in the production of neoprene elastomers, is of regulatory interest due to the production of multi-organ tumors in mouse and rat cancer bioassays. A significant increase in female mouse lung tumors was observed at the lowest exposure concentration of 12.8 ppm while a small, but not statistically significant, increase was observed in female rats only at the highest exposure concentration of 80 ppm. The metabolism of chloroprene results in the generation of reactive epoxides and the rate of overall chloroprene metabolism is highly species dependent. To identify potential key events in the mode-of-action of chloroprene lung tumorigenesis, dose response and time course gene expression microarray measurements were made in the lungs of female mice and female rats. The gene expression changes were analyzed using both a traditional analysis of variance approach followed by pathway enrichment analysis and a pathway-based benchmark dose (BMD) analysis approach. Pathways related to glutathione biosynthesis and metabolism were the primary pathways consistent with cross-species differences in tumor incidence and transcriptional BMD values for the pathway were more similar to differences in tumor response than were estimated target tissue dose surrogates based on the total amount of chloroprene metabolized per unit mass of lung tissue per day. The closer correspondence of the transcriptional changes with the tumor response are likely due to their reflection of the overall balance between metabolic activation and detoxication reactions whereas the current tissue dose surrogate reflects only oxidative metabolism. Female mice (B6C3F1/Crl) were exposed to chloroprene (CAS 126-99-8) by whole-body inhalation exposure at 0, 0.3, 2, 13, or 90 ppm. Exposures were performed for 6 hr/day, 5 days per week. The animals were sacrified at 5 days or 19 days (15 exposure days) post initiation of exposure. The right lung was excised and gene expression microarray analysis was performed using Affymetrix Mouse 430_2 arrays. Female rats (F344/NCrl) were exposed to chloroprene (CAS 126-99-8) by whole-body inhalation exposure at 0, 5, 30, 90, or 200 ppm. Exposures were performed for 6 hr/day, 5 days per week. The animals were sacrified at 5 days or 19 days (15 exposure days) post initiation of exposure. The right lung was excised and gene expression microarray analysis was performed using Affymetrix Rat 230_2 arrays.
2012-10-12 | E-GEOD-40795 | biostudies-arrayexpress
Project description:We study differences in gene expression between Populus P35S::BL (BL-oe) lines and control, affecting plant growth and differentiation, and dormancy. We used microarrays to detail the global program of gene expression underlying morphological and developmental changes droved by overexpression of BL gene. We identified an activation tagging mutant with increased leaf size and correspondingly name it BIG LEAF (BL). We positioned the tag, localized a putative candidate gene and verified transcription activation. The activated gene encodes a WD40 putative transcription regulator similar to the Arabidopsis thaliana STERILE APETALA (SAP). We recapitulated the phenotype by overexpression of the gene into the same genotype under strong constitutive promoter (P35S::BL, BL-oe). Transgenic up-regulation of the BL gene caused enhanced leaf size, early bud-break, and suppression of secondary growth. BL transcript abundance in wild type plants is in apical tissues, mostly in shoot meristem, leaf primordia and axillary meristem. Our data indicates that BL plays an important role in the process of tree growth. Poplar apex, secondary stem (30th internode), and leaves (at 30 node) was selected for RNA extraction and hybridization on Affymetrix microarrays. We sought to obtain expression of affected genes in P35S::BL lines and control wild type (WT-717), in order to increase the resolution of expression profiles inducing the developmental changes in P35S::BL. To do that, we selected apex, stem and leaf tissue from greenhouse healthy plants.
2017-05-11 | E-GEOD-68859 | biostudies-arrayexpress