Mus musculus strain:C57BL/6J
Ontology highlight
ABSTRACT:
PROVIDER: PRJDB17212 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| DRR520547_1.fastq.gz | Fastqsanger.gz | |||
| DRR520547_2.fastq.gz | Fastqsanger.gz | |||
| DRR520548_1.fastq.gz | Fastqsanger.gz | |||
| DRR520548_2.fastq.gz | Fastqsanger.gz | |||
| DRR520549_1.fastq.gz | Fastqsanger.gz |
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Project description:Analysis of gene expression in lungs of C57BL/6J mice that develop chronic airway disease phenotypes after a single Sendai virus infection, compared with mice treated with UV-inactivated virus. Keywords: disease state analysis
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Project description:Analysis of gene expression in lungs of C57BL/6J mice that develop chronic airway disease phenotypes after a single Sendai virus infection, compared with mice treated with UV-inactivated virus. Keywords: disease state analysis
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Project description:Analysis of gene expression in lungs of C57BL/6J mice that develop chronic airway disease phenotypes after a single Sendai virus infection, compared with mice treated with UV-inactivated virus. Keywords: disease state analysis
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Project description:We hypothesize that gene expression in the aging lungs of these two strains of mice are divergent thus contributing to the disparity in the phenotypes.re specifically, (1) Aging DBA/2J mice compared to aging C57BL/6 mice are known to be accelerated in their lung physiology andrphometry; (2) C57BL/6J are known to have longer natural longevity than DBA/2J mice. In order to test these hypotheses at the gene expression level, we utilized microarray analysis to examine transcriptional differences between aging lungs of both strains of mice. Experiment Overall Design: This study utilizes microarray analysis to test these hypotheses. Three sets of lungs were harvested from both strains at each time point (C57BL/6J: 2, 18, AND 26s; DBA/2J: 2 and 18s). RNA was isolated and used for global gene expression profiling (Affymetrixuse 430 2.0 array). Statistically significant gene expression was determined as a minimum 6 counts of 9 pairwise comparisons, minimum 1.5-fold change, and p < 0.05. Further, Absolute | FC - FC SEM | >= 1.5.
2009-04-23 | E-GEOD-6591 | biostudies-arrayexpress
Project description:We hypothesize that gene expression in the aging lungs of these two strains of mice are divergent thus contributing to the disparity in the phenotypes. More specifically, (1) Aging DBA/2J mice compared to aging C57BL/6 mice are known to be accelerated in their lung physiology and morphometry; (2) C57BL/6J are known to have longer natural longevity than DBA/2J mice. In order to test these hypotheses at the gene expression level, we utilized microarray analysis to examine transcriptional differences between aging lungs of both strains of mice. Keywords: comparative expression profiling
2007-08-31 | GSE6591 | GEO
Project description:Analysis of gene expression in lungs of C57BL/6J mice that develop chronic airway disease phenotypes after a single Sendai virus infection, compared with mice treated with UV-inactivated virus. Keywords: disease state analysis Whole lung RNA was analyzed from 3 mice per condition per time point 49 days post infection, Sendai virus versus UV-inactivated virus, C57BL/6J mouse strain.
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Project description:Analysis of gene expression in lungs of C57BL/6J mice that develop chronic airway disease phenotypes after a single Sendai virus infection, compared with mice treated with UV-inactivated virus. Keywords: disease state analysis Whole lung RNA was analyzed from 3 mice per condition per time point 3 days post infection, Sendai virus versus UV-inactivated virus, C57BL/6J mouse strain.
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Project description:Single-nucleus RNA sequencing of neonatal and adult mice after spinal cord injury
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Project description:Intrahepatic cholestasis of pregnancy (ICP) is estimated to impact between 0.4% and 5% of pregnancies worldwide. This disease is associated with elevated maternal bile acids and frequently untoward neonatal outcomes such as respiratory distress and asphyxia. Multiple candidate genes have been implicated, but none have provided insight into the mechanisms of neonatal respiratory distress and death. Herein our studies demonstrate that maternal cholestasis (due to Abcb11 deficiency) produces 100% neonatal death within 24h due to atelectasis producing pulmonary hypoxia, which recapitulates the respiratory distress and asphyxia of human ICP. We show that these neonates have elevated pulmonary bile acids that are associated with disrupted structure of pulmonary surfactant. Maternal absence of Nr1i2 superimposed upon Abcb11 deficiency strongly increased neonatal survival and is directly related to reduced maternal bile acid concentrations. The mechanism accounting for reduced serum bile acids in the mothers deficient in both Nr1i2 and Abcb11 appears related to disrupted reabsorption of intestinal bile acids due to changes in transporter expression. These findings provide novel insights into pulmonary failure by revealing bile acids capability to disrupt the structure of surfactant producing collapsed alveoli, pulmonary failure and ultimately death. These findings have important implications for neonatal health especially when maternal bile acids are elevated during pregnancy and highlight a potential pathway and targets amenable to therapeutic intervention to ameliorate this condition. We used microarrays to measure changes in gene expression profiles in lung tissues from Abcb11+/- lungs after interbreeding C57BL/6 wild-type female or C57BL/6 Abcb11-/- female mice against either C57BL/6 wild-type male mice or C57BL/6 Abcb11-/- male mice to create only heterozygote offspring. We also measured profiles in liver tissues from age-matched C57BL/6 wild-type and C57BL/6 Abcb11-/- mice. Lung tissues were collected from day E17.5, E18.5 and neonatal (N0) mice. Liver tissues were collected from 1.5-month-old C57BL/6 wildtype and Abcb11-/- mice.
2015-09-23 | E-GEOD-70179 | biostudies-arrayexpress
Project description:Defects in homocysteine and folate metabolism are associated with increased risks for neural tube and congenital heart defects, cardiovascular disease and stroke, cancers, and neurodegeneration. In many but not all cases, dietary supplementation with folate significantly reduces the severity and incidence of these conditions. Common polymorphisms modulate these metabolic pathways and disease risks, but do not fully account for the particular birth defects and adult diseases that occur in at-risk individuals. To test whether other pathways contribute to disease pathogenesis, we analyzed global and pathway-specific changes in gene expression and levels of selected metabolites after depletion and repletion of dietary folate in two genetically distinct inbred strains of mice. Compared to the C57BL/6J strain, A/J showed greater homeostatic response to folate perturbation by retaining a higher serum folate level and minimizing global gene expression changes. Remarkably, folate perturbation led to systematic strain-specific differences only in the expression profile of the cholesterol biosynthesis pathway and translated to changes in levels of serum and liver total cholesterol. By genetically increasing serum and liver total cholesterol levels in APOE deficient mice, we modestly but significantly improved folate retention during folate depletion, suggesting an interplay between homocysteine and folate metabolism and cholesterol metabolism. Absence of measurable changes in global methylation patterns or amelioration of effects with supplementation with an alternative methyl donor suggest that dietary folate perturbations do not act through large-scale or general changes in methylation. These results suggest that homeostatic responses in cholesterol metabolism contribute to the beneficial effects of dietary folate supplementation. Keywords: time course, stress response, diet, genetic, homeostasis
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