BACKGROUND: Peroxisome proliferator-activated receptor g (PPAR g) is a nuclear receptor whose activation has been shown to modulate macrophage and epithelial cell-mediated inflammation. The objective of this study was to use a systems approach for investigating the mechanism by which the deletion of PPAR g in T cells modulates the severity of dextran-sodium sulfate (DSS)-induced colitis, immune cell distribution and global gene expression.
The role of T cell PPAR gamma in mice with experimental inflammatory bowel disease.
No sample metadata fields
View SamplesBACKGROUND: Peroxisome proliferator-activated receptor g (PPAR g) is a nuclear receptor whose activation has been shown to modulate macrophage and epithelial cell-mediated inflammation. The objective of this study was to use a systems approach for investigating the mechanism by which the deletion of PPAR g in epithelial cells modulates the severity of dextran-sodium sulfate (DSS)-induced colitis, immune cell distribution and global gene expression.
Immunoregulatory actions of epithelial cell PPAR gamma at the colonic mucosa of mice with experimental inflammatory bowel disease.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Response of gastric epithelial progenitors to Helicobacter pylori Isolates obtained from Swedish patients with chronic atrophic gastritis.
Age, Specimen part, Treatment
View SamplesHelicobacter pylori infection is associated with development of gastric adenocarcinoma in a subset of infected humans, especially those that develop an antecedent condition, chronic atrophic gastritis (ChAG) characterized by loss of acid-producing parietal cells. Studies in a gnotobiotic transgenic mouse model of ChAG, with an engineered ablation of parietal cells and an associated expansion of gastric epithelial progenitors (GEPs), have shown that a subset of GEPs is able to harbor intracellular collections of H. pylori. To better understand H. pyloris adaptation to ChAG, we sequenced the genomes of 24 isolates, obtained from 6 individuals, each sampled over a 4-year interval, as they maintained normal gastric histology, or progressed from normal histology to ChAG, or experienced worsening ChAG, or proceeded from ChAG to cancer. Analyses of gene content and single nucleotide polymorphisms (SNPs) demonstrated that H. pylori populations within study participants were largely clonal, and remarkably stable over the 4-year interval, regardless of disease state. Because they exhibited such broad inter-host variation (38.64.7 SNPs/1000bp of genome), and did not cluster according to host pathology, we sought to identify common functional properties by performing GeneChip studies of the responses of a cultured mouse gastric stem cell-like line (mGEPs) to infection with sequenced strains. The results yielded a shared 695-member set of genes differentially expressed after infection with ChAG-associated, but not normal or heat killed strains: 434 of these genes were also represented in dataset of responses to the cancer-associated strain. Ingenuity Pathway Analysis revealed that ChAG- and ChAG/cancer- associated responses were significantly enriched in genes associated with tumorigenesis in general, and gastric carcinogenesis in specific cases. Whole genome transcriptional profiling of a sequenced ChAG strain during mGEP infection disclosed a set of responses that included upregulation of hopZ, an adhesin belonging to a family of outer membrane proteins. Expression profiles of wild-type and hopZ strains revealed a number of pH-regulated genes affected by loss of HopZ, including HopP which binds sialylated glycans produced by GEPs in vivo. Genetic inactivation of hopZ produces a fitness defect in gnotobiotic transgenic mice but not their wild-type littermates. This study illustrates an approach for identifying GEP responses specific to ChAG, and bacterial genes important for survival in a gastric ecosystem that lacks parietal cells.
Response of gastric epithelial progenitors to Helicobacter pylori Isolates obtained from Swedish patients with chronic atrophic gastritis.
Age, Specimen part, Treatment
View SamplesDepletion of essential nutrients triggers regulatory programs that prolong cell growth and survival. Starvation-induced processes increase nutrient transport, mobilize nutrient storage, and recycle nutrients between cellular components. This leads to an effective increase in intracellular nutrients, which may act as a negative feedback that down-regulates the starvation program. To examine how cells overcome this potential instability, we followed the transcription response of budding yeast transferred to medium lacking phosphate. Genes were induced in two temporal waves. The first wave was stably maintained and persisted even upon phosphate replenishment, indicating a positive feedback loop. This commitment was abolished after two hours with the induction of the second expression wave, coinciding with the reduction in cell growth rate. We identify genes that mediate this loss of commitment, and show that the overall temporal stability of the expression response depends on the sequential pattern of gene induction. Our results emphasize the key role of gene expression dynamics in optimizing cellular adaptation. Wild type cells were grown at high Phosphate medium, washed and transferred to no phosphate medium. Sample were taken every 15 minuets for 6 hours Overall design: 25 samples were taken during the time course. Expression data was normalized to the first time point (cells grown at high phosphate medium)
Sequential feedback induction stabilizes the phosphate starvation response in budding yeast.
Genetic information, Subject
View SamplesDepletion of essential nutrients triggers regulatory programs that prolong cell growth and survival. Starvation-induced processes increase nutrient transport, mobilize nutrient storage, and recycle nutrients between cellular components. This leads to an effective increase in intracellular nutrients, which may act as a negative feedback that down-regulates the starvation program. To examine how cells overcome this potential instability, we followed the transcription response of budding yeast transferred to medium lacking phosphate. Genes were induced in two temporal waves. The first wave was stably maintained and persisted even upon phosphate replenishment, indicating a positive feedback loop. This commitment was abolished after two hours with the induction of the second expression wave, coinciding with the reduction in cell growth rate. We identify genes that mediate this loss of commitment, and show that the overall temporal stability of the expression response depends on the sequential pattern of gene induction. Our results emphasize the key role of gene expression dynamics in optimizing cellular adaptation. Wild type cells were grown at high Phosphate medium, washed and transferred to no phosphate medium. Sample were taken every 15 minuets for 6 hours Overall design: 25 samples were taken during the time course. Expression data was normalized to the first time point (cells grown at high phosphate medium)
Sequential feedback induction stabilizes the phosphate starvation response in budding yeast.
Genetic information, Subject
View SamplesDepletion of essential nutrients triggers regulatory programs that prolong cell growth and survival. Starvation-induced processes increase nutrient transport, mobilize nutrient storage, and recycle nutrients between cellular components. This leads to an effective increase in intracellular nutrients, which may act as a negative feedback that down-regulates the starvation program. To examine how cells overcome this potential instability, we followed the transcription response of budding yeast transferred to medium lacking phosphate. Genes were induced in two temporal waves. The first wave was stably maintained and persisted even upon phosphate replenishment, indicating a positive feedback loop. This commitment was abolished after two hours with the induction of the second expression wave, coinciding with the reduction in cell growth rate. We identify genes that mediate this loss of commitment, and show that the overall temporal stability of the expression response depends on the sequential pattern of gene induction. Our results emphasize the key role of gene expression dynamics in optimizing cellular adaptation. Wild type cells were grown at high Phosphate medium, washed and transferred to no phosphate medium. Sample were taken every 15 minuets for 6 hours Overall design: 25 samples were taken during the time course. Expression data was normalized to the first time point (cells grown at high phosphate medium)
Sequential feedback induction stabilizes the phosphate starvation response in budding yeast.
Genetic information, Subject
View SamplesDepletion of essential nutrients triggers regulatory programs that prolong cell growth and survival. Starvation-induced processes increase nutrient transport, mobilize nutrient storage, and recycle nutrients between cellular components. This leads to an effective increase in intracellular nutrients, which may act as a negative feedback that down-regulates the starvation program. To examine how cells overcome this potential instability, we followed the transcription response of budding yeast transferred to medium lacking phosphate. Genes were induced in two temporal waves. The first wave was stably maintained and persisted even upon phosphate replenishment, indicating a positive feedback loop. This commitment was abolished after two hours with the induction of the second expression wave, coinciding with the reduction in cell growth rate. We identify genes that mediate this loss of commitment, and show that the overall temporal stability of the expression response depends on the sequential pattern of gene induction. Our results emphasize the key role of gene expression dynamics in optimizing cellular adaptation. Wild type cells were grown at high Phosphate medium, washed and transferred to no phosphate medium. Sample were taken every 15 minuets for 6 hours Overall design: 25 samples were taken during the time course. Expression data was normalized to the first time point (cells grown at high phosphate medium)
Sequential feedback induction stabilizes the phosphate starvation response in budding yeast.
Genetic information, Subject
View SamplesDepletion of essential nutrients triggers regulatory programs that prolong cell growth and survival. Starvation-induced processes increase nutrient transport, mobilize nutrient storage, and recycle nutrients between cellular components. This leads to an effective increase in intracellular nutrients, which may act as a negative feedback that down-regulates the starvation program. To examine how cells overcome this potential instability, we followed the transcription response of budding yeast transferred to medium lacking phosphate. Genes were induced in two temporal waves. The first wave was stably maintained and persisted even upon phosphate replenishment, indicating a positive feedback loop. This commitment was abolished after two hours with the induction of the second expression wave, coinciding with the reduction in cell growth rate. We identify genes that mediate this loss of commitment, and show that the overall temporal stability of the expression response depends on the sequential pattern of gene induction. Our results emphasize the key role of gene expression dynamics in optimizing cellular adaptation. Wild type cells were grown at high Phosphate medium, washed and transferred to no phosphate medium. Sample were taken every 15 minuets for 6 hours Overall design: 25 samples were taken during the time course. Expression data was normalized to the first time point (cells grown at high phosphate medium)
Sequential feedback induction stabilizes the phosphate starvation response in budding yeast.
Genetic information, Subject
View SamplesDepletion of essential nutrients triggers regulatory programs that prolong cell growth and survival. Starvation-induced processes increase nutrient transport, mobilize nutrient storage, and recycle nutrients between cellular components. This leads to an effective increase in intracellular nutrients, which may act as a negative feedback that down-regulates the starvation program. To examine how cells overcome this potential instability, we followed the transcription response of budding yeast transferred to medium lacking phosphate. Genes were induced in two temporal waves. The first wave was stably maintained and persisted even upon phosphate replenishment, indicating a positive feedback loop. This commitment was abolished after two hours with the induction of the second expression wave, coinciding with the reduction in cell growth rate. We identify genes that mediate this loss of commitment, and show that the overall temporal stability of the expression response depends on the sequential pattern of gene induction. Our results emphasize the key role of gene expression dynamics in optimizing cellular adaptation. Wild type cells were grown at high Phosphate medium, washed and transferred to no phosphate medium. Sample were taken every 15 minuets for 6 hours Overall design: 25 samples were taken during the time course. Expression data was normalized to the first time point (cells grown at high phosphate medium)
Sequential feedback induction stabilizes the phosphate starvation response in budding yeast.
Genetic information, Subject
View Samples