Here we examined virulence activation in Pseudomonas aeruginosa in response to the synthetic kappa opioid agonist U-50, 488 in nutrient poor media where growth conditions are limited and density dependent quorum sensing is not activated.
Pseudomonas aeruginosa overrides the virulence inducing effect of opioids when it senses an abundance of phosphate.
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View SamplesWe report bulk RNAseq of in vitro cultured horizontal basal cells, and in vivo isoalted respiratory basal cells of the murine olfactory epithelium, and compared their profiles with pre-existing bulk RNAseq of in vivo isolated HBCs and single cell RNAseq of in vivo HBCs. Overall design: RNAseq of in vitro horizontal basal cells (HBCs) in triplicate under control conditions, and FACS isolated in vivo respiratory basal cells in singlet
Activating a Reserve Neural Stem Cell Population In Vitro Enables Engraftment and Multipotency after Transplantation.
Subject
View SamplesTopoisomerase 1 (TOP1) poisons like camptothecin (CPT), which are used as chemotherapeutic agents in cancer, elicit DNA damage in quiescient neurons. In this study, we examined the effects of CPT and actinomycin D (ActD) on neuronal cells. Motor (MNs) and cortical (CNs) neurons were more susceptible to the toxic effects of CPT and ActD than fibroblasts. MNs and CNs exhibited a delayed DNA damage responseincrease in nuclear -H2AX focirelative to fibroblasts. Neuronal cells expressed higher levels of Top1 mRNA than fibroblasts which could explain their enhanced vulnerability to CPT and ActD toxicity. Microarray analysis was performed to identify differentially regulated transcripts in MNs treated with CPT for 2 hours. Many immediate-early genes including Fos and Egr-1 were upregulated in CPT-treated MNs. Fos mRNA levels were elevated in all cells types treated with CPT; Egr-1 transcript levels, however, were reduced in CPT-treated fibroblasts even though they were elevated in treated MNs and CNs. Pathway and network analysis of the differentially expressed transcripts revealed activation of ERK and JNK signaling cascades in CPT-treated MNs. In conclusion, MNs were more vulnerable than fibroblasts to the damaging effects of TOP1 poisons and they elicit a unique intracellular response to CPT treatment.
Identification of early gene expression changes in primary cultured neurons treated with topoisomerase I poisons.
Specimen part, Treatment
View SamplesWe have performed genome-wide DNA methylation analysis at single base resolution and gene expression analysis, resulted in hypermethylation in all autosomes in DS samples, mediated by down-regulation of all three TET family genes, and down-regulation of REST/NRSF. Genes located on chr21 were up-regulated by a median of 45% in DS compared to normal villi, while genes with promoter hypermethylation were down regulated. Overall design: Comparison of RNA expression in human placenta between 5 normal and 4 Trisomy 21 samples.
Global DNA hypermethylation in down syndrome placenta.
Specimen part, Subject
View SamplesThis SuperSeries is composed of the SubSeries listed below.
ACSL1 Is Associated With Fetal Programming of Insulin Sensitivity and Cellular Lipid Content.
Sex
View SamplesWe hypothesised that SGA as a proxy for intrauterine growth restriction promotes specific epigenetic marks and pathways, whose physiological implications may become apparent only in the fully differentiated state.
ACSL1 Is Associated With Fetal Programming of Insulin Sensitivity and Cellular Lipid Content.
Sex
View SamplesWe hypothesised that SGA as a proxy for intrauterine growth restriction promotes specific epigenetic marks and pathways, whose physiological implications may become apparent only in the fully differentiated state.
ACSL1 Is Associated With Fetal Programming of Insulin Sensitivity and Cellular Lipid Content.
Sex
View SamplesMutations in the parkin gene, which encodes a ubiquitin ligase, are a major genetic cause of parkinsonism. Interestingly, parkin also plays a role in cancer as a putative tumor suppressor, and the gene is frequently targeted by deletion and inactivation in human malignant tumors. Here, we investigated a potential tumor suppressor role for parkin in gliomas. We found that parkin expression was dramatically reduced in glioma cells. Restoration of parkin expression promoted G1 phase cell cycle arrest and mitigated the proliferation rate of glioma cells in vitro and in vivo. Notably, parkin-expressing glioma cells showed a reduction in levels of cyclin D1, but not cyclin E, and a selective downregulation of Akt serine-473 phosphorylation and VEGF receptor levels. In accordance, cells derived from a parkin null mouse model exhibited increased levels of cyclin D1, VEGF receptor and Akt phosphorylation and divided significantly faster when compared with wild type cells, with suppressionof these changes following parkin re-introduction. Clinically, analysis of parkin pathway activation was predictive for the survival outcome of glioma patients. Taken together, our study provides mechanistic insight into the tumor suppressor function of parkin in brain tumors, and suggests that measurement of parkin pathway activation may be used clinically as a prognostic tool in brain tumor patients.
Parkin pathway activation mitigates glioma cell proliferation and predicts patient survival.
Cell line, Treatment
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Molecular pathways reflecting poor intrauterine growth are found in Wharton's jelly-derived mesenchymal stem cells.
Specimen part
View SamplesIn order to identify gene-expression patterns in mesenchymal stem cells associated with different birth weights and intrauterine growth parameters,
Molecular pathways reflecting poor intrauterine growth are found in Wharton's jelly-derived mesenchymal stem cells.
Specimen part
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