Although a number of animal model studies have addressed changes in gene expression in the parenchyma and their relationship to emphysema, much less is known about the pathogenesis of cigarette smoke-induced small airway remodeling. In this study, we exposed rat tracheal explants to whole smoke for 15 minutes, and then cultured the explants in air. The airway transcriptome was evaluated using RAE 230_2 GeneChips. By 2 hours after starting smoke exposure, expression levels of 502 genes were changed up or down by more than 1.5 times (p values <0.01 or less), and by 24 hours, 1870 genes were significantly changed up or down. These included genes involved in anti-oxidant protection, epithelial defense and remodeling, inflammatory mediators and transcription factors, and a number of unexpected genes including the MMP-12 inducer, tachykinin-1 (substance P). Pre-treatment of the explants with 1 x 10-7 M dexamethasone reduced the number of significantly changed genes by approximately 47% at 2 hr and 68% at 24 hours, and in almost all instances, reduced the magnitude of the smoke-induced changes. We conclude that even a very brief exposure to cigarette smoke can lead to rapid changes in the expression of a large number of genes in rat tracheal explants, and that these effects are directly mediated by smoke, without a need for exogenous inflammatory cells. Steroids, contrary to the usual belief, are able to ameliorate many of these changes, at least in this very acute model.
Modification of the rat airway explant transcriptome by cigarette smoke.
Specimen part, Treatment
View SamplesBackground
Distinct roles of the Gcn5 histone acetyltransferase revealed during transient stress-induced reprogramming of the genome.
Treatment
View SamplesWe report gene expression in human neutrophils isolated by two methods: Polymorphprep (~95% purity) and negative selection (~99% purity) from two healthy donors - one donor with low eosinophil contamination of neutrophils and one donor with high eosinophil contamination of neutrophils. We report the effect of the presence of contaminating leukocytes in neutrophil preparations, and in reponse to inflammatory cytokines TNF-alpha and GM-CSF. Overall design: Healthy human neutrophils were isolated using Polymorphprep or negative selection, and incubated for 1h in the absence or presence of TNF-alpha or GM-CSF. RNA was analysed by Illumina HiSeq 2000. The results from n=2 donors were analysed as biological replicates for differential expression analysis.
Whose Gene Is It Anyway? The Effect of Preparation Purity on Neutrophil Transcriptome Studies.
No sample metadata fields
View SamplesThe data provide information expression profile in yeast for 5 different physioloigcal conditions during stress adpatation and stress recovery (normal growth, during stress adaptation, after stress adaptation, under stress recovery, after stress recovery) in yeast. The purpose of the study is to understand how histone acetyltransferase HATs (Gcn5) apply it is function in gene regulation by changing global or local histone acetylation level under different physiological conditions.
Distinct roles of the Gcn5 histone acetyltransferase revealed during transient stress-induced reprogramming of the genome.
Treatment
View SamplesNeutrophils are known to be stimulated by different periodontal bacteria to produce reactive oxygen species and cytokines. It is inportant to investigate the gene changes made by bacteria of importance, of which, for periodontal disease, fusobaterium nucleatum is one. we used microarrays to investigate gene experssion changes in peripheral blood neutrophils werwhich e stimulated with or with out Fusobacterium Nucleatum (10953).
Fusobacterium nucleatum regulation of neutrophil transcription.
Specimen part
View SamplesA new method for amplification and labeling of RNA is assessed that permits gene expression microarray analysis of formalin-fixed paraffin embedded tissue (i.e. FFPET) samples.
A novel method of amplification of FFPET-derived RNA enables accurate disease classification with microarrays.
Specimen part, Treatment
View SamplesMost individuals with cystic fibrosis (CF) carry one or two mutations that result in a maturation defect of the full-length CFTR protein. The deltaF508 mutation results in a mutant protein that is degraded by the proteasome instead of progressing to the apical membrane where it functions as a cyclic AMP-regulated chloride channel. 4 phenylbutyrate modulates heat shock protein expression and promotes trafficking of deltaF508 thus permitting maturation and membrane insertion. The goal of this study was to gain insight into the genetic mechanism of PBA action through a large-scale analysis of gene expression. The Affymetrix genome spanning U133 microarray set was used to compare mRNA expression in untreated IB3-1 cell line cultures with cultures treated with 1mM 4-phenylbuyterate for 12 and 24 hr. IB3-1 deltaF508/W1282X) bronchial epithelial cells were cultured in T75 flasks with gentamicin-free LHC-8 medium. Cells were fed with 10 ml of media every 2 to 3 days. After reaching 80% confluence cells were treated with 1 mM PBA. A T75 flask of confluent IB3-1 cells was rinsed twice with ice cold Hanks buffer then scraped into 3ml of ice cold TRIzol (Gibco BRL) then rinsed with 3 ml ice cold TRIzol and the mRNA was isolated according to the TRIzol protocol. A total of 5 control cultures, 3 cultures with 12 hr BPA application and 3 cultures with 24 hr PBA application were processed
Gene expression profile analysis of 4-phenylbutyrate treatment of IB3-1 bronchial epithelial cell line demonstrates a major influence on heat-shock proteins.
No sample metadata fields
View SamplesFollowing myocardial infarction, the prognosis for females is better than males. Estrogen is thought to be protective, but clinical trials with hormone replacement failed to show protection. Here, we sought to identify novel mechanisms that might explain this sex-based difference. By diverging from the traditional focus on sex hormones, we employed a conceptually novel approach to this question by using a non-biased approach to measure global changes in gene expression following infarction.
An association between gene expression and better survival in female mice following myocardial infarction.
Sex, Specimen part
View SamplesGene expression analysis of hypothalami from female animals at different juvenile developmental reproductive stages. Results provide insight into the role of the hypothalamus in controlling the onset of puberty. Overall design: SD rats were housed (8/cage) in a controlled environment and euthanized at different ages (PND=7, PND=14, Early Juvenile: 21 days, Late Juvenile: 28 days, Late Proestus (the day of first ovulation): 30-33 days. Rats were anesthetized and brains were rapidly removed. The medial basal hypothalamus (MBH) was dissected away from the rest of the brain and flash frozen. Total RNA was isolated from each sample using Qiagen''s RNeasy Mini Kit (Valencia, CA). Samples were bioanalyzed on a RNA 6000 Nano chip kit to check for integrity and concentration before sending it to OHSU''s Massively Parallel Sequencing Shared Resource for library preparation and sequencing.
Trithorax dependent changes in chromatin landscape at enhancer and promoter regions drive female puberty.
No sample metadata fields
View SamplesModerate alcohol consumption during pregnancy can result in a heterogeneous range of neurobehavioural and cognitive effects, termed fetal alcohol spectrum disorders (FASD). We have developed a mouse moder of FASD that involves moderate ethanol exposure throughout gestation achieved by voluntary maternal consumption. This model results in phenotypes relevant to FASD. Since ethanol is known to directly affect the expression of genes in the developing brain leading to abnormal cell death, changes to cell proliferation, migration, and differentiation, and potential changes to epigenetic patterning, we hypothesize that this leaves a long-term footprint on the adult brain. However, the long-term effects of prenatal ethanol exposure on brain gene expression, when behavioural phenotypes are apparent, are unclear.
Long-term alterations to the brain transcriptome in a maternal voluntary consumption model of fetal alcohol spectrum disorders.
Treatment
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