Wistar rats, purchased from BRL (Fullinsdorf/BL, Switzerland), and WBN/Kob rats, purchased from SLC Inc. (Shizuoka, Japan), were specific pathogen-free. Rats were housed in groups of maximally 4 instandard cages (1,820 cm2 bottom area) and kept in our animal facility for various time periods between 1 week and 36 weeks (free access to standard rat chow and water; specific pathogen-free conditions; 20 degree C; day/night cycle simulated by artificial lighting of 50 lx from 7 a.m. to 7 p.m., dimmed in the remaining hours to almost complete darkness; air humidity 50 to 60%). Prior to surgery or sacrifice, the rats were fasted overnight (16 to18 h) with free access to water. All manipulations conformed with the Swiss Federal Guidelines on Animal Experiments and were approved by the local ethics committee.
Inflammation-dependent expression of SPARC during development of chronic pancreatitis in WBN/Kob rats and a microarray gene expression analysis.
Sex, Age, Specimen part, Time
View SamplesRight ventricular samples were serially acquired during surgical repair of ventricular septal defect. Expression profiling revealed three patterns of gene expression: (1) increased expression above control levels within one hour of cardioplegic arrest, with further amplification during early reperfusion; (2) increased expression limited to the reperfusion phase; and (3) reduced expression during reperfusion.
Early gene expression profiles during intraoperative myocardial ischemia-reperfusion in cardiac surgery.
No sample metadata fields
View SamplesWhile human embryonic stem cells (hESCs) are predisposed towards chromosomal aneploidities on 12, 17, 20 and X, rendering them susceptible to transformation, the specific genes expressed are not yet known. Here, by identifying the genes over expressed in pluripotent rhesus ESCs (nhpESCs) and comparing them to both their genetically-identical differentiated progeny (teratoma fibroblasts) as well as genetically-related differentiated parental cells (parental skin fibroblasts from whom gametes were used for ESC derivation), we find that some of those over expressed genes in nhpESCs cluster preferentially on rhesus chromosomes 16, 19, 20 and X, homologues of human chromosomes 17, 19, 16 and X respectively. Differentiated parental skin fibroblasts display gene expression profiles closer to nhpESC profiles than to teratoma cells, which are genetically identical to the pluripotent nhpESCs. Twenty over and under expressed pluripotency modulators, some implicated in neurogenesis, have been identified. The over expression of some of these genes discovered using pedigreed nhpESCs derived from prime embryos generated by fertile primates, which is impossible to perform with the anonymously donated clinically-discarded embryos from which hESCs are derived, independently confirms the importance of chromosome 17 and X regions in pluripotency and suggests specific candidates for targeting differentiation and transformation decisions.
Pluripotency genes overexpressed in primate embryonic stem cells are localized on homologues of human chromosomes 16, 17, 19, and X.
Specimen part
View SamplesPedigreed primate ESCs display homogeneous and reliable expression profiles.
Pedigreed primate embryonic stem cells express homogeneous familial gene profiles.
No sample metadata fields
View SamplesMethylene diphenyl diisocyanate is a chemical known to cause asthma. The present study uses mice to investigate exposure-induced changes in lung gene expression and effects of a chloride channel inhibitor
Analysis of Lung Gene Expression Reveals a Role for Cl<sup>-</sup> Channels in Diisocyanate-induced Airway Eosinophilia in a Mouse Model of Asthma Pathology.
Sex
View SamplesWe hypothesized that gene expression in lungs of Fra-1+/+ and Fra-1-/- mice are divergent thus contributing fibrosis. More specifically, Fra-1-/- mice are increased susceptible to fibrosis. In order to test these hypotheses at the gene expression level, we utilized microarray analysis to examine transcriptional differences between Fra-1+/+ and Fra-1-/- mice at early time point.
Expression profiling of genes regulated by Fra-1/AP-1 transcription factor during bleomycin-induced pulmonary fibrosis.
Sex, Age, Specimen part
View SamplesRATIONALE: 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.
Genetic and pharmacologic evidence links oxidative stress to ventilator-induced lung injury in mice.
No sample metadata fields
View SamplesWe hypothesize that gene expression in the Type II cells of Nrf2+/+ and Nrf2-/- mice are divergent thus contributing the cell growth. More specifically, type II cells from Nrf2-/- mice have increased reactive oxygen species that cause the impaired cell growth. In order to test these hypotheses at the gene expression level, we utilized microarray analysis to examine transcriptional differences between Nrf2+/+ and Nrf2-/- cells.
Genetic dissection of the Nrf2-dependent redox signaling-regulated transcriptional programs of cell proliferation and cytoprotection.
No sample metadata fields
View SamplesAnalysis of genes regulated by STC1 down-regulation in mouse 4T1 derived clone, 4T1ch9. STC1 expression is associated with tumor growth and metastasis. This study looks at genes affected when STC1 expression is down-regulated by STC1 shRNA.
STC1 expression is associated with tumor growth and metastasis in breast cancer.
Cell line
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Genome-wide transcriptomic analysis of cotton under drought stress reveal significant down-regulation of genes and pathways involved in fibre elongation and up-regulation of defense responsive genes.
Specimen part, Treatment
View Samples