The purpose of this study was to assess transcriptome changes in primary human airway epithelial cells following stimulation with RIG-I ligand. Overall design: MRNA profiles were generated from primary human airway epithelial cells at rest or following stimulation with RIG-I ligand SLR-14.
Regional Differences in Airway Epithelial Cells Reveal Tradeoff between Defense against Oxidative Stress and Defense against Rhinovirus.
Specimen part, Treatment, Subject
View SamplesThe purpose of this study was to assess transcriptome changes in primary human airway epithelial cells following stimulation with RIG-I ligand. Overall design: MRNA profiles were generated from primary human airway epithelial cells at rest or following stimulation with RIG-I ligand.
Regional Differences in Airway Epithelial Cells Reveal Tradeoff between Defense against Oxidative Stress and Defense against Rhinovirus.
Specimen part, Treatment, Subject
View SamplesRecent work using mouse models has revealed that mTORC2, which unlike mTORC1 is not acutely sensitive to rapamycin, plays a key role in the regulation of organismal physiology. The substrates and pathways regulated by mTORC2 are at present relatively unknown
Hepatic signaling by the mechanistic target of rapamycin complex 2 (mTORC2).
Sex, Specimen part, Treatment
View SamplesThe goal of the current study was to identify changes in gene expression in the stomach muscularis that may be contributing to altered gastric motility in gastroparesis and obesity. Overall design: Stomach muscularis biopsies were obtained from human subjects with low BMI and normal gastric motility (low BMI control, n=6), subjects with high BMI but normal gastric motility (high BMI control, n=6), subjects with low BMI and gastroparesis (low BMI gastroparesis, n=6) and from subjects with high BMI and gastroparesis (High BMI gastroparesis, n=4). RNA was isolated and subjected to whole transcriptome sequencing.
Transcriptome profiling reveals significant changes in the gastric muscularis externa with obesity that partially overlap those that occur with idiopathic gastroparesis.
Specimen part, Subject
View SamplesThis SuperSeries is composed of the SubSeries listed below.
AMPK and PPARdelta agonists are exercise mimetics.
No sample metadata fields
View SamplesExercise activates serine/threonine kinase AMPK and transcriptional factor PPARdelta that re-model metabolism and endurance capacity of skeletal muscle. Whether and how synthetic activation of these molecules regulated muscle gene signature is unknown.
AMPK and PPARdelta agonists are exercise mimetics.
No sample metadata fields
View SamplesExercise training increases endurance by inducing global gene expression changes in skeletal muscles. The extent to which the genetic effects of exercise can be mimicked by synthetic drugs is unknown.
AMPK and PPARdelta agonists are exercise mimetics.
No sample metadata fields
View SamplesThe goal of this project is to generate transcriptome profiling of intestinal stem cells for a systemic analysis of cellular pathways involved in responses to fasting. Overall design: Examination of one cell type in two conditions.
Fasting Activates Fatty Acid Oxidation to Enhance Intestinal Stem Cell Function during Homeostasis and Aging.
Age, Specimen part, Cell line, Subject
View SamplesLittle is known about how pro-obesity diets regulate tissue stem and progenitor cell function. Here we find that high fat diet (HFD)-induced obesity augments the numbers and function of Lgr5+ intestinal stem cells (ISCs) of the mammalian intestine. Like HFD, ex vivo treatment of intestinal organoid cultures with palmitic acid (PA), a constituent of the HFD, enhances the self-renewal potential of these organoid bodies. Mechanistically, HFD induces a robust peroxisome proliferator-activated receptor delta (PPAR-delta signature in intestinal stem and progenitor cells and pharmacologic activation of PPAR-delta recapitulates the effects that HFD has on these cells. Interestingly, HFD- and agonist-activated PPAR-delta signaling endows organoid-initiating capacity to non-stem cells and enforced PPAR-delta signaling permits these non-stem cells to form in vivo tumors upon loss of the tumor suppressor Apc. These findings highlight how diet-modulated PPAR-delta activation alters not only the function of intestinal stem and progenitor cells but also their capacity to initiate tumors. Overall design: mRNA profiles of intestinal stem cells (GFP-Hi) and progenitors (GFP-Low) from WT or HFD fed mice were generated by deep sequencing using HiSeq 2000.
High-fat diet enhances stemness and tumorigenicity of intestinal progenitors.
No sample metadata fields
View SamplesWe report that developmental competition between sympathetic neurons for survival is critically dependent on a sensitization process initiated by target innervation and mediated by a series of feedback loops. Target-derived nerve growth factor (NGF) promoted expression of its receptor TrkA in neurons and prolonged TrkA-mediated signals. NGF also controlled expression of brain derived neurotrophic factor (BDNF) and neurotrophin-4 (NT4), which, through the receptor p75, can kill neighboring neurons with low retrograde NGFTrkA signaling whereas neurons with high NGFTrkA signaling are protected. Perturbation of any of these feedback loops disrupts the dynamics of competition. We suggest that three target-initiated events are essential for rapid and robust competition between neurons: sensitization, paracrine apoptotic signaling, and protection from such effects.
A model for neuronal competition during development.
No sample metadata fields
View Samples