Oxidative stress is a hallmark of inflammation in infection or sterile tissue injury. We show that partially oxidized phospholipids of microvesicles (MVs) from plasma of patients with rheumatoid arthritis or cells exposed to oxidative stress induce activation of TLR4. MVs from healthy donors or reconstituted synthetic MVs can be converted to TLR4 agonists by limited oxidation, while prolonged oxidation abrogates the activity. Activation by MVs mimics the mechanism of TLR4 activation by LPS. However, LPS and MVs induce significantly different transcriptional response profile in mouse BMDMs with a strong inflammation-resolving component induced by the endogenous signals. MVs thus represent a ubiquitous endogenous danger signal released under the oxidative stress, which underlies the pervasive role of TLR4 signaling in inflammation.
Toll-like receptor 4 senses oxidative stress mediated by the oxidation of phospholipids in extracellular vesicles.
Sex
View SamplesAmong colicin producing E. coli, colicin M producing strains are the most frequently present in natural populations. Bacteria must be able to sense and respond to unfavourable conditions, resulting in adaptive responses. To gain insight into colicin M ecological role and the purposes related to antimicrobial therapy, the effects of subinhibitory concentrations of colicin M on E. coli whole genome transcription was investigated. We used microarray analysis to follow differential gene expression in E. coli upon colicin M exposure. Colicin M inhibits peptidoglycan synthesis altering expression of genes involved in envelope stress, osmotic and other stresses, exopolysaccharide prodoction, biofilm formation, and cell motility.
Global transcriptional responses to the bacteriocin colicin M in Escherichia coli.
Treatment
View SamplesA 30-day nutritional trial in broiler chickens (Ross 308) was conducted to investigate how specific forms of vitamin E (α- and γ-tocopherol) and their combination impact liver gene expression when oxidative susceptibility of the organism is induced by high n-3 polyunsaturated fatty acids (PUFA) intake. Thirty-six one-day-old male broilers were fed a diet enriched with 5 % linseed oil to induce oxidative susceptibility. Beside negative (N) and positive (P) control group, experimental groups were supplemented with either: 67 mg/kg RRR-α-tocopherol (A), 67 mg/kg RRR-γ-tocopherol (G) or with combination of 33.5 mg/kg of each tocopherol (S). Whole chicken genome microarray analysis was performed on liver RNA and selected differentially expressed genes were confirmed by qRT-PCR.
No associated publication
Sex, Specimen part, Compound
View SamplesThis SuperSeries is composed of the SubSeries listed below.
The human primary hepatocyte transcriptome reveals novel insights into atorvastatin and rosuvastatin action.
Specimen part, Subject, Time
View SamplesAffymetrix gene expression profiling in cumulus cells (CC) retrieved from patients undergoing GnRH agonists and GnRH antagonists IVF treatment.
Cumulus cells gene expression profiling in terms of oocyte maturity in controlled ovarian hyperstimulation using GnRH agonist or GnRH antagonist.
Subject
View SamplesWith particular emphasis on interactions between cholesterol homeostasis and drug metabolism we investigate the transcriptome of human primary hepatocytes treated by two commonly prescribed cholesterol lowering drugs atorvastatin and rosuvastatin and by rifampicin that serves as an outgroup as well as a model substance for induction of nuclear receptor PXR.
The human primary hepatocyte transcriptome reveals novel insights into atorvastatin and rosuvastatin action.
Specimen part, Subject, Time
View SamplesThis SuperSeries is composed of the SubSeries listed below.
No associated publication
Specimen part, Time
View SamplesCholesterol is one of the key molecules in mammals and the most striking examples of its deficiency are the inborn errors of cholesterol biosynthesis that manifest in severe whole body phenotypes. Liver, the principal site of cholesterol homeostasis, has rarely been investigated in these defects. We thus focused on the hepatocyte-specific deletion of lanosterol 14-demethylase (CYP51) catalyzing the rate-limiting step in the post-squalene part of cholesterol synthesis.
Lessons from hepatocyte-specific Cyp51 knockout mice: impaired cholesterol synthesis leads to oval cell-driven liver injury.
Sex, Specimen part, Treatment
View SamplesUnperturbed cholesterol homeostasis is important for normal development and sexual maturation in mice. Cyp51 is the rate limiting step in the post-lanosteorl part of cholesterol biosynthesis. Unlike the full body knockout, hepatocyte specific Cyp51 knockout mice survive throughout adulthood, however their livers are severly affected. Several of the hepatocyte specific Cyp51 knockout mice develop severe liver injury or die prior to reaching adulthood (from 4-10 weeks of age; designated as runts). We aim to uncover the timing and the mechanistic background governing the liver damage and sex differences.
Disrupting Hepatocyte Cyp51 from Cholesterol Synthesis Leads to Progressive Liver Injury in the Developing Mouse and Decreases RORC Signalling.
Sex, Specimen part
View SamplesThe current study was designed to clarify signalling pathways and assess possible beneficial effect of new probiotic mixture in DSS (dextran sulphate sodium) induced colitis mouse model. Manipulation of intestinal microbiota with probiotics represents a promising alternative or adjunct therapy in gastrointestinal disorders and inflammation.
No associated publication
Sex, Specimen part, Disease, Treatment
View Samples