Expression profiling of rapidly-induced genes upon VSV infection at 4 hours post-infection in Drosophila cells
Transcriptional pausing controls a rapid antiviral innate immune response in Drosophila.
Cell line
View SamplesTo determine the Cdk9 targets of VSV-induced genes in Drosophila cells at 4 hours post-infection
Transcriptional pausing controls a rapid antiviral innate immune response in Drosophila.
Cell line, Treatment
View SamplesWe use the zebrafish embryo model to study the transcriptome responses to flagellin and Pam3CSK4. Therefore, we injected these PAMPs into the caudal vein at the 27 hours post fertilization and took samples at 1 hour post injection. Overall design: This deep sequence study was designed to determine the gene expression profile by Pam3CSK4 and flagellin injection. RNA was isolated from embryos at 1 hour post injection. Wildtypes and tlr2- and tlr5a- morphants zebrafish embryos were micro-injected into the caudal vein with 1ng of Pam3CSK4, 0,1 ng flagellin , or water as a control at 27 hours post fertilization. After injections embryos were transferred into fresh egg water and incubated at 28°C. At 1 hour post injection triplicates of 10 to 15 embryos per condition were snap-frozen in liquid nitrogen, and total RNA was isolated using TRIZOL reagent.
Biological clock function is linked to proactive and reactive personality types.
No sample metadata fields
View SamplesBackground: Heat stress triggers an evolutionarily conserved set of responses in cells. The transcriptome responds to hyperthermia by altering expression of genes to adapt the cell or organism to survive the heat challenge. RNA-seq technology allows rapid identification of environmentally responsive genes on a large scale. In this study, we have used RNA -seq to identify heat stress responsive genes in the chicken male white-leghorn hepat ocellular (LMH) cell line. Result: The transcripts of 812 genes were responsive to heat stress (p <0.01) with 235 genes up- regulated and 577 down-regulated following 2.5 hours of heat stress. Among the up- regulated were genes whose products function as chaperones, along with genes aff ecting collagen synthesis and deposition, transcription factors, chromatin remodelers and genes modulating the WNT and TGF-beta pathways. Predominant among the down-regulated genes were ones that affect DNA replication and repair along with chromosom al segregation. Many of the genes identified in this study have not been previously implicated in the heat stress response. Conclusion: These data extend our understanding of the transcriptome response to heat stress. Many of the identified biological processes and pathways likely function in adapting cells and organisms to hyperthermic stress. This study may provide important guides to future efforts attempting to improve species abilities to withstand heat stress through genome wide association studies and breeding. In addition, the genes down regulated by heat stress may provide important targets for improving hyperthemic treatment in cancer patients. Overall design: Cells were grown at either control ( 37oC) or heat stress (43oC) temperatures for 2.5 hours.
Transcriptome response to heat stress in a chicken hepatocellular carcinoma cell line.
Cell line, Treatment, Subject
View SamplesCellular RNA levels are determined by transcription and decay rates, which are fundamental in understanding gene expression regulation. Measurement of these two parameters is usually performed independently, complicating analysis and introducing methodological biases that hamper direct comparison. Here, we present a simple approach of concurrent sequencing of S. cerevisiae polyA+ and polyA- RNA 3' ends to simultaneously estimate total RNA levels, transcription and decay rates from the same RNA sample. The transcription data generated correlate well with reported estimates and also reveal local RNA polymerase stalling and termination sites with high precision. Although the method by design uses brief metabolic labeling of newly synthesized RNA with 4-thiouridine, the results demonstrate that transcription estimates can also be gained from unlabeled RNA samples. These findings underscore the potential of the approach, which should be generally applicable to study a range of biological questions in diverse organisms. Overall design: RNA 3' end seq of total and 2min 4-thiouracil (4tU) labelled RNA from S. cerevisiae cells. Aliquots of RNA were directly subjected to pA+ RNA 3' end sequencing (noPap samples). A second aliquot was in vitro polyadenylated using E. coli poly(A) polymerase and ribodepleted before library preparation (xPap samples).
Simultaneous Measurement of Transcriptional and Post-transcriptional Parameters by 3' End RNA-Seq.
Cell line, Subject
View SamplesWe hypothesize that gene expression in the CS-exposed lungs of this strain (A/J) of mice would be able to give clues about the molecular mechanism of emphysema development, thus contributing to this phenotype. More specifically, although imbalance in oxidants/antioxidants and proteinase/antiproteinase pathways drives the pathogenesis of COPD, the molecular mechanisms involved in the development of emphysema are poorly understood. In order to test this hypothesis at the gene expression level, we utilized microarray analysis to examine transcriptional differences between CS-exposed and Air-exposed groups of mice.
Cigarette smoke-induced emphysema in A/J mice is associated with pulmonary oxidative stress, apoptosis of lung cells, and global alterations in gene expression.
Sex, Age, Specimen part
View SamplesExperiments in rodents have shown that kidney ischemia/reperfusion injury (IRI) facilitates lung injury and inflammation. To identify potential ischemia-specific lung molecular pathways involved, we conducted global gene expression profiling of lung 6 or 36 hours following 1) bilateral kidney IRI, 2) bilateral nephrectomy (BNx), and 3) sham laparotomy in C57BL/6J mice. Total RNA from whole lung was isolated and hybridized to 430MOEA (22,626 genes) GeneChips (n=3/group).
Ischemic acute kidney injury induces a distant organ functional and genomic response distinguishable from bilateral nephrectomy.
No sample metadata fields
View SamplesWe hypothesize that gene expression in the cigarette smoke (CS) exposed neonatal lung and age-matched controls will be divergent. CS exposed lung will have divergence of immune response genes and structural genes. The lungs of (6) 2 week old neonatal mice exposed to 2 weeks of CS were compared to the lung of (4) 2 week old age-matched control mice. We utilized microarray analysis to examine transcriptional differences between smoke exposed neonatal lung and age-matched controls.
Impaired lung homeostasis in neonatal mice exposed to cigarette smoke.
No sample metadata fields
View SamplesGoblet cell metaplasia and mucus hypersecretion are disabling hallmarks of chronic lung diseases for which no curative treatments are available. Therapies targeting specific upstream drivers of asthma have had variable results. We hypothesized that an a priori-knowledge independent approach would point to new therapies for airway goblet cell metaplasia. We analyzed the transcriptome of an organotypic model of human goblet cell metaplasia. We combined our data with previously published datasets from IL13-exposed in vitro and asthmatic in vivo human airway epithelial cells. The drug perturbation-response connectivity approach identified the heat shock protein 90 (HSP90) inhibitor geldanamycin as a candidate for reverting airway goblet cell metaplasia. We found that geldanamycin not only prevented but reverted IL13-induced goblet cell metaplasia. Geldanamycin did not induce goblet cell death, did not solely block mucin synthesis, and did not block IL13 receptor-proximal signaling. Moreover, the transcriptional effects of geldanamycin were absent in unstimulated cells and became evident only after stimulation with IL13. The predicted mechanism of action suggested that geldanamycin should also revert IL17-induced goblet cell metaplasia, a prediction confirmed by our data. Our findings suggest HSP90 activity may be required for persistence of goblet cell metaplasia driven by various mechanisms in chronic lung diseases. Overall design: For both batches, airway epithelia cultures from the lungs of eight different humans were studied, therefore, there are eight biological replicates. Comparisons should be made within batches. In batch 1 (XAM1), epithelia were exposed to vehicle (DMSO 0.5%), geldanamycin 25 uM, or the HDAC6 inhibitor ISOX 10 uM for 48 hours. In batch 2 (XAM3), the epithelia were exposed to vehicle (DMSO 0.5%), IL13 (20 ng/mL) or IL13 plus geldanamycin (10 uM) for 48 hours.
HSP90 inhibitor geldanamycin reverts IL-13- and IL-17-induced airway goblet cell metaplasia.
Specimen part, Treatment, Subject
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Protective role of IL-6 in vascular remodeling in Schistosoma pulmonary hypertension.
Sex, Specimen part, Disease, Disease stage, Treatment
View Samples