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SRP127589
Saccharomyces cerevisiae
26 Downloadable Samples
Illumina HiSeq 2500
Description
Cellular 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).
Publication Title
Simultaneous Measurement of Transcriptional and Post-transcriptional Parameters by 3' End RNA-Seq.
Sample Metadata Fields
Cell line, Subject
View Samples- Mus musculus
- 21 Downloadable Samples
Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
We 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.
Publication Title
Cigarette smoke-induced emphysema in A/J mice is associated with pulmonary oxidative stress, apoptosis of lung cells, and global alterations in gene expression.
Sample Metadata Fields
Sex, Age, Specimen part
View Samples- Mus musculus
- 20 Downloadable Samples
- Affymetrix Mouse Expression 430A Array (moe430a)
Description
Experiments 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).
Publication Title
Ischemic acute kidney injury induces a distant organ functional and genomic response distinguishable from bilateral nephrectomy.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 10 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
We 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.
Publication Title
Impaired lung homeostasis in neonatal mice exposed to cigarette smoke.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 6 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Protective role of IL-6 in vascular remodeling in Schistosoma pulmonary hypertension.
Sample Metadata Fields
Sex, Specimen part, Disease, Disease stage, Treatment
View Samples- Mus musculus
- 12 Downloadable Samples
- Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)
Description
RATIONALE: Mechanical ventilation (MV) is an indispensable therapy for critically ill patients with acute lung injury and the adult respiratory distress syndrome. However, the mechanisms by which conventional MV induces lung injury remain unclear. OBJECTIVES: We hypothesized that disruption of the gene encoding Nrf2, a transcription factor which regulates the induction of several antioxidant enzymes, enhances susceptibility to ventilator-induced lung injury (VILI), while antioxidant supplementation attenuates such effect. METHODS: To test our hypothesis and to examine the relevance of oxidative stress in VILI, here we have assessed lung injury and inflammatory responses in Nrf2-deficient (Nrf2(-/-)) mice and wildtype (Nrf2(+/+)) animals following acute (2 h) injurious model of MV with or without administration of antioxidant. MEASUREMENTS AND MAIN RESULTS: Nrf2(-/-) mice displayed greater levels of lung alveolar and vascular permeability and inflammatory responses to MV as compared to Nrf2(+/+) mice. Nrf2-deficieny enhances the levels of several pro-inflammatory cytokines implicated in the pathogenesis of VILI. We found diminished levels of critical antioxidant enzymes and redox imbalance by MV in the lungs of Nrf2(-/-) mice; however antioxidant supplementation to Nrf2(-/-) mice remarkably attenuated VILI. When subjected to clinically relevant prolong period of MV, Nrf2(-/-) mice displayed greater levels of VILI than Nrf2(+/+) mice. Expression profiling revealed lack of induction of several VILI genes, stress response and solute carrier proteins and phosphatases in Nrf2(-/-) mice. CONCLUSIONS: Collectively, our data demonstrate for the first time a critical role for Nrf2 in VILI, which confers protection against cellular responses induced by MV by modulating oxidative stress.
Publication Title
Genetic and pharmacologic evidence links oxidative stress to ventilator-induced lung injury in mice.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 6 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
Rationale: Schistosomiasis is one of the most common causes of pulmonary arterial hypertension worldwide, but the pathogenic mechanism by which the host inflammatory response contributes to vascular remodeling is unknown. We sought to identify signaling pathways that play protective or pathogenic roles in experimental Schistosoma-induced pulmonary vascular disease by whole-lung transcriptome analysis. Methods: Wildtype mice were experimentally exposed to S. mansoni ova by intraperitoneal sensitization followed by tail vein augmentation, and the phenotype assessed by right ventricular catheterization and tissue histology, RNA and protein analysis. Whole-lung transcriptome analysis by microarray and RNA sequencing was performed, the latter analyzed using 2 bioinformatic methods. Functional testing of the candidate IL-6 pathway was determined using IL6-knockout mice and the STAT3 inhibitor STI-201. Results: Wild-type mice exposed to S. mansoni had increased right ventricular systolic pressure and thickness of the pulmonary vascular media. Whole lung transcriptome analysis identified the IL6-STAT3-NFATc2 pathway as being upregulated, which was confirmed by PCR and immunostaining of lung tissue from S. mansoni-exposed mice and patients who died of the disease. Mice lacking IL6 or treated with STI-201 developed pulmonary hypertension associated with significant intima remodeling after exposure to S. mansoni. Conclusions: Whole lung transcriptome analysis identified upregulation of the IL6-STAT3-NFATc2 pathway, and IL6 signaling was found to be protective against Schistosoma-induced intimal remodeling.
Publication Title
Protective role of IL-6 in vascular remodeling in Schistosoma pulmonary hypertension.
Sample Metadata Fields
Sex, Specimen part, Disease, Disease stage, Treatment
View Samples- Drosophila melanogaster
- 3 Downloadable Samples
- Affymetrix Drosophila Genome 2.0 Array (drosophila2)
Description
Expression profiling of rapidly-induced genes upon VSV infection at 4 hours post-infection in Drosophila cells
Publication Title
Transcriptional pausing controls a rapid antiviral innate immune response in Drosophila.
Sample Metadata Fields
Cell line
View Samples- Drosophila melanogaster
- 3 Downloadable Samples
- Affymetrix Drosophila Genome 2.0 Array (drosophila2)
Description
To determine the Cdk9 targets of VSV-induced genes in Drosophila cells at 4 hours post-infection
Publication Title
Transcriptional pausing controls a rapid antiviral innate immune response in Drosophila.
Sample Metadata Fields
Cell line, Treatment
View Samples- Danio rerio
- 21 Downloadable Samples
- IlluminaHiSeq2500
Description
We 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.
Publication Title
Biological clock function is linked to proactive and reactive personality types.
Sample Metadata Fields
No sample metadata fields
View Samples