Darwin Tree of Life - COPO submission
Ontology highlight
ABSTRACT:
SUBMITTER:
PROVIDER: S-BIAD904 | bioimages |
REPOSITORIES: bioimages
Similar Datasets
Project description:The Genotype-Tissue Expression (GTEx) project v8
2024-02-24 | E-GTEX-8 | ExpressionAtlas
Project description:Transcription profiling of aerial parts of Arabidopsis wild type and arr10 arr12 double mutant seedlings treated with the cytokinin trans-zeatin
2015-06-10 | E-NASC-75 | ExpressionAtlas
Project description:RNA-sequencing of 465 lymphoblastoid cell lines from the 1000 Genomes
2019-07-15 | E-GEUV-1 | ExpressionAtlas
Project description:Transcription profiling by array of Arabidopsis after treatment with oligogalacturonides
2015-06-10 | E-NASC-76 | ExpressionAtlas
Project description:Bisphenol A (BPA) is a xenobiotic endocrine disrupting chemical. In vitro and in vivo studies indicated that BPA alters endocrine-metabolic pathways in adipose tissue increasing the risk of developing metabolic disorders. BPA effects on human adipocytes, specifically in children, are poorly investigated. To investigate in childhood the effect of exposure to BPA on metabolic disorders we analyzed in vitro the effects of environmentally relevant doses of BPA on gene expression of mature human adipocytes from pre-pubertal lean patients and on related physiological outcomes. Adipocytes from children were treated in vitro with BPA and gene expression was evaluated by qRT-PCR. Genome wide analyses were performed using GeneChip Human Gene 1.0 ST array. Lipid content in adipocytes was estimated by ORO staining and Triglyceride Quantification Kit. Secreted IL-1beta, in adipocytes culture medium, and insulin, in PANC-1 culture medium, were performed using ELISA assays. BPA was found to promote up-regulation of ERα and ERRγ, and down-regulation of GPR30 expression modulating estrogen signaling and following a non-linear dose-response. Microarray data analysis demonstrated that BPA increases the gene expression of pro-inflammatory cytokines and lipid metabolism-related FABP4 and CD36 in adipocytes. PCSK1 resulted the most interesting gene being down-regulated by BPA thus impairing insulin production in pancreas. BPA promotes inflammation and lipid metabolism dysregulation in adipocytes from lean children. Moreover, PCSK1 can be a key gene in BPA action modulating insulin production. Exposure to BPA in childhood may be an important risk factor in developing obesity and metabolic disorders. Three prototypic situations were analyzed (5 replication each): untreated cells (C), 10 nM BPA treated cells (BPA), 1 nM 17-beta Estradiol treated cells (ES).
2015-09-18 | E-GEOD-58516 | ExpressionAtlas
Project description:Pharmacological activation of the transcription factor PPAR gamma lowers blood pressure and improves glucose tolerance in humans. In contrast, naturally occurring mutations (e.g., P467L, V290M) in the ligand binding domain of PPAR gamma in humans leads to severe insulin resistance and early-onset hypertension. Experimental evidence, including whole genome expression profiling, suggests that these mutant versions of PPAR gamma act in a dominant negative manner. Because PPAR gamma is expressed in a variety of cell types and tissues, we generated a transgenic mouse model (SP467L) specifically targeting dominant negative PPAR gamma to the vascular smooth muscle cells in order to determine the action of PPAR gamma in the blood vessel independent of its systemic metabolic actions. In the data set provided herein, we examined the gene expression profile in thoracic aorta from SP467L mice and their control littermates using the Affymetrix mouse exon 1.0 ST array. We generated transgenic mice specifically targeting expression of mutant dominant negative human PPAR gamma (P467L) to vascular smooth muscle using a smooth muscle-specific promoter (smooth muscle myosin heavy chain or SMMHC). Thoracic aortas were isolated from 7 male transgenic mice and 5 non-transgenic littermate controls. Total RNA was prepared using conventional methods and quality was assessed using the Bioanalyzer 2100 (Agilent Technologies). For the microarray hybridizations, each sample corresponded to aorta derived from one mouse. All procedures were conducted at the University of Iowa DNA Core facility using standard Affymetrix protocols. In brief, approximately 50 ng of total RNA was used as input to a two-step amplification procedure (NuGen, http://www.nugeninc.com/) to generate biotin-labeled RNA fragments for hybridization to the Affymetrix mouse exon 1.0 ST array.
2015-09-28 | E-GEOD-37195 | ExpressionAtlas
Project description:Transcription profiling by array of rat kidney from animals with low, normal or high blood pressure
2014-08-16 | E-MIMR-541 | ExpressionAtlas
Project description:Transcription profiling by array of mouse embryonic stem cells expressing the transcription factor NGN3 for 12 hours, 24 hours and 48 hours
2014-07-03 | E-MIMR-461 | ExpressionAtlas
Project description:Transcription profiling by array of Drosophila larvae after parasitoid attack
2014-08-01 | E-MAXD-6 | ExpressionAtlas
Project description:The present study aimed to delineate the central mechanisms by which androgens delay wound repair. Blocking the conversion of testosterone to 5alpha-dihydrotestosterone (DHT) by 5alpha-reductase limits its ability to impair skin wound healing, suggesting that DHT is a more potent inhibitor of repair than is testosterone. This study aims to identify, through transcription profiling, potential mechanisms by which the 5alpha-reductase inhibitor MK-434 modulates repair. Microarray analysis of wound RNA samples from rats in which the transformation of testosterone to DHT is prevented has identified biological processes and key individual genes through which DHT may contribute to the altered healing profile in such animals. These include genes with putative roles in wound contraction and re-epithelialization.
2015-10-22 | E-MEXP-1232 | ExpressionAtlas