Transcription profiling of mice treated with hypoxia and/or sleep fragmentation to investigate the hypothesis that intermittent hypoxia may lead to upregulation of some novel peptide(s) that have a powerful glucose lowering action
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ABSTRACT:
ORGANISM(S): Mus musculus
SUBMITTER: Eric Hoffman
PROVIDER: E-GEOD-480 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:Study the gene expression variation at cerebral cortex using two mouse model strains (C57BL/6 and ApoE(-/-) on the C57BL background) upon episode hypoxia treatment
2013-01-30 | E-TIGR-135 | biostudies-arrayexpress
Project description:Why we sleep is still one of the most perplexing mysteries in biology. Strong evidence, however, indicates that sleep is necessary for normal brain function and that the need to sleep is a tightly regulated process. Surprisingly molecular mechanisms that determine the need to sleep are incompletely described. Moreover, very little is known about transcriptional changes that specifically accompany the accumulation and discharge of sleep need. In this study we present an integrated 2 cross-laboratory analysis of the effects of sleep deprivation (SD) in gene expression in the mouse cortex. We also evaluate changes in gene expression genome-wide following various lengths of subsequent recovery sleep. (RS). We demonstrate that changes in gene expression specifically linked to SD or RS, and not to technical factors (e.g. the assay used), requires a novel analysis methodology not previously utilized in the field of sleep research. Cortical samples from mice were analyzed, from groups that were sleep deprived, sleep deprived and allowed to recover for 1, 2, 3, or 6 hours, and circadian control animals that were not sleep deprived. The experimental protocol began at lights on (ZT0) with 13 mice: 1 sacrificed, 4 control mice left undisturbed, and 8 mice kept awake with gentle brushing when attempting to sleep. After 5 hours of sleep deprivation the mice were randomly assigned to recovery sleep or continued sleep deprivation, and at fixed intervals the mice were sacrificed, dissected and the left cortex retained. The experimental protocol was repeated 7 times, one animal per timepoint per experimental day, so that 7 independent experiments are represented for each timepoint. All animals were acclimated to the brushing and tapping on cages used during sleep deprivationfor 6 days, and dissections and tissue collection were performed by a single experimenter.
2016-09-07 | E-GEOD-78215 | biostudies-arrayexpress
Project description:Obesity is a chronic inflammatory disease that weakens macrophage innate immune response to infections. Since M1 polarization is crucial during acute infectious diseases, we hypothesized that diet-induced obesity inhibits M1 polarization of macrophages in the response to bacterial infection. Using a computational approach in conjunction with microarray data, we identified switching genes that may differentially control the behavior of response pathways in macrophages from lean and obese mice. Bone marrow macrophages (BMMM-NM-&) from lean and obese mice were exposed to live Porphyromonas gingivalis (P. gingivalis) for three incubation times (1 h, 4 h and 24 h). cDNA from BMMM-NM-& of lean and obese mice were hybridized on Affymetrix Mouse Genome 430 2.0 Arrays. Hybridization was performed on three replicates at each time point (18 arrays total).
2013-06-12 | E-GEOD-47414 | biostudies-arrayexpress
Project description:Effect of miR-122 silencing in diet induced obese mice.
2008-03-27 | E-MEXP-1406 | biostudies-arrayexpress
Project description:To address whether hypoxia contributes to muscle patho-physiology, normal, adult C57 mice were exposed to chronic, normobaric and hypobaric hypoxic environments for 2 weeks in order to simulate levels of hypoxaemia reported in DMD patients with advanced respiratory insufficiency. Control mice were maintained under normoxic conditions. Control and experimental mice were studied. Experiment Overall Design: Adult male C57Bl/10 mice were used in experiments. At the beginning of the experiment mice were divided into two groups, control (room condition) and hypoxic (hypoxic condition), over a period of 2 weeks. The hypoxic group was gradually exposed to lower levels of hypoxia in an especially designed and hermetically closed hypoxic chamber. A Pegas 4000 MF(Columbus Instruments) gas blending system was used. The oxygen level was gradually decreased from 21% to 8% over one week and animals were kept at 8% oxygen for another 7 days. Animalâs weights were monitored daily. Food and water were changed daily for the time of the experiment. After two weeks animals were euthanized using CO2, Extensor digitorum longus (EDL) and Soleus muscles were dissected for physiological studies. Prior to physiological analysis each group was divided into two smaller groups (subgroups). In the first subgroup the primary focus on physiological muscle analysis was on (EDL) while in the other subgroup it was on Soleus. This division allowed us that both muscles, EDL and Soleus were analyzed at the same time after euthanization. Experiment Overall Design: RNA isolation Experiment Overall Design: Total RNA was isolated from each QF muscle by Tri-Reagent (Ambion, Austin, TX) as described by manufacturer. Isolated total RNA were cleaned up by RNeasy mini kit (Qiagen, Valencia, CA) as described by manufacturer. The purity and concentration of total RNA were determined by measurement of absorbance at 260 and 280nm using a Nanodrop ND-1000 spectrophotometer (NanoDrop Technologies, Wilmington, DE). To satisfy our purity criteria, we discarded all RNA samples that did not have a 260/280 ratio between 1.8 and 2.1. To satisfy our criteria for integrity, we required that all RNA used in our experiments have single peaks for the 18S and 28S bands as determined by the Agilent 2100 Bioanalyzer (Agilent Technologies Inc., Palo Alto, CA). Experiment Overall Design: Linear amplification and cRNA labeling Experiment Overall Design: Three microliter total RNA was used for each sample to obtain linearly amplified labeled cRNA by using GeneChip® One-Cycle Target Labeling kit (Affymetrix, Santa Clara, CA) as manufacturer described. Briefly; total RNA was used to generate double-stranded cDNA with the T7-oligo (dT) primer. This double-stranded cDNA was used in vitro transcription and biotin labeling steps. Labeled cRNA yield and purity were determined by measuring the absorbance at 260 and 280nm. All the cRNA 260/280 ratios were between 1.9 and 2.1. Quality control (QC) of the labeled cRNA products was assessed by performing 1µg labeled cRNA on 2% agarose gel to see similar RNA smear type. Experiment Overall Design: Fragmentation and microarray hybridization Experiment Overall Design: Fifteen micrograms labeled cRNA of hypoxic or normoxic QF muscle was fragmented, and 10μg was hybridized to Affymetrix® Mouse 430 ver 2.0 GeneChip arrays for 18â24h (Affymetrix Inc.). Each microarray was washed and stained with streptavidinâphycoerythrin and scanned at a 6-μm resolution with Agilent model G2500A GeneArray scanner A visual quality control measurement was performed to ensure proper hybridization after each chip was scanned.
2009-10-20 | E-GEOD-9400 | biostudies-arrayexpress
Project description:Despite considerable progress understanding genes that affect the HDL particle, its function, and cholesterol content, genes identified to date explain only a small percentage of the genetic variation. We used N-ethyl-N-nitrosourea mutagenesis in mice to discover novel genes that affect HDL cholesterol levels. Two mutant lines (Hlb218 and Hlb320) with low HDL cholesterol levels were established. Causal mutations in these lines were mapped using linkage analysis: For line Hlb218 within a 12 Mbp region on Chr 10; and for line Hlb320 within a 17 Mbp region on Chr 7. High-throughput sequencing of Hlb218 liver RNA identified a mutation in Pla2g12b. The transition of G to A leads to a cysteine to tyrosine change and most likely causes a loss of a disulfide bridge. Microarray analysis of Hlb320 liver RNA showed a 7-fold downregulation of Hpn; sequencing identified a mutation in the 3M-bM-^@M-2 splice site of exon 8. Northern blot confirmed lower mRNA expression level in Hlb320 and did not show a difference in splicing, suggesting that the mutation only affects the splicing rate. In addition to affecting HDL cholesterol, the mutated genes also lead to reduction in serum non-HDL cholesterol and triglyceride levels. Despite low HDL cholesterol levels, the mice from both mutant lines show similar atherosclerotic lesion sizes compared to control mice. These new mutant mouse models are valuable tools to further study the role of these genes, their affect on HDL cholesterol levels, and metabolism. Mutant mice were generated as part of The Jackson LaboratoryM-bM-^@M-^Ys Heart, Lung, Blood, and Sleep Disorder Mutagenesis Program by treating male C57BL/6J (B6) mice with N-ethyl-N-nitrosourea (ENU). Third generation (G3) mice were phenotyped to ensure capture of both dominant and recessive mutations. Two unique G3 animals with low HDL cholesterol levels were then used to establish new inbred lines (Hlb218 and Hlb320) by mating them with B6 mice and intercrossing the offspring with low HDL cholesterol for 7 generations. Livers from 3 Hlb218, 3 Hlb320 males, and 6 B6 male controls were obtained for gene expression analysis. The samples were randomized over Illumina Mouse-6 Expression 1.1 BeadChips .
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Project description:We used microarrays to detail the global programme of gene expression underlying the effect of sleep deprivation in the mouse hippocampus and identified distinct classes of regulated genes during this process. Hippocampal tissue was taken from sleep deprived mice and time-matched non-sleep-deprived control animals that were left undisturbed in their home cages during the sleep deprivation period for a total of 8 and 9 replicates per group. RNA was isolated and cDNA was synthesized from hippocampal tissue, and the sample from each animal was hybridized to a separate Affymetrix Mouse 430_2 microarray
2012-09-06 | E-GEOD-33302 | biostudies-arrayexpress
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2009-08-19 | E-MEXP-2201 | biostudies-arrayexpress
Project description:Time-course gene expression profiles were obtained from lung tissues of the rats treated with room air, intermittent- (IH) or sustained hypoxia (SH) for 1, 3, 7, 14 and 30 days using CodeLink microarrays. Using a systems biology approach, we observed that two different mechanisms are involved in the lung responses to IH and SH: IH leads to increased G-protein coupled signaling-, ion transport-, neuronal- and steroid hormone receptor activities; whereas SH causes increased blood vessel morphogenesis and immune responses. Our results provide insight into molecular mechanisms underlying IH and SH. Keywords: gene expression array-based, count rats were treated with intermittent- (IH) or sustained hypoxia (SH) for 1, 3, 7, 14 and 30 days; rats treated with room air were used as controls; gene expression profiles were obtained from these rats
2008-12-17 | E-GEOD-8705 | biostudies-arrayexpress
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2015-07-08 | E-GEOD-69079 | biostudies-arrayexpress