E-GEOD-34424
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: PRJNA149553
PROVIDER: E-GEOD-34424 | ExpressionAtlas | 2015-07-27
REPOSITORIES: ExpressionAtlas
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| E-GEOD-34424-analysis-methods.tsv | Tabular | |||
| E-GEOD-34424-atlasExperimentSummary.Rdata | Rdata | |||
| E-GEOD-34424-configuration.xml | Xml | |||
| E-GEOD-34424-percentile-ranks.tsv | Tabular | |||
| E-GEOD-34424.condensed-sdrf.tsv | Tabular |
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Similar Datasets
Project description:The Influence of Sleep Deprivation on Hippocampal CA1 Gene Expression: Relation to Stress and Aging
| PRJNA149553 | ENA
Project description:Sleep deprivation (SD) in young adults is associated with metabolic, stress and cognitive responses that are also characteristic of brain aging. Given that sleep architecture changes with age, including increased fragmentation and decreased slow wave activity, it seems reasonable to investigate potential molecular relationships between SD and aging in brain tissue. Here, we tested the hypothesis that young rats exposed to 24 or 72 hour SD would respond with stress and aging-like shifts in brain hippocampal CA1 gene expression. SD animals showed blood corticosterone and weight changes consistent with a stress response. Microarray results, validated by Western blot and comparison to prior SD studies, pointed to disruptions in neurotransmission, sleep pressure signaling, and macromolecular synthesis. In a separate experiment, animals exposed to 24 or 72 hour novel environment stress recapitulated nearly one third of the SD transcriptional profile, particularly upregulated apoptotic and immune signaling pathways. Compared to aging (based on three previously published independent hippocampal aging studies), SD transcriptional profiles agreed for neurogenesis and energy pathways. However, immune signaling, glial activity, macromolecular synthesis and neuronal function all showed an SD profile that was, at least in part, opposed by aging. We conclude that while stress and SD have discrete molecular signatures, they do show a subset of highly similar changes. However, the same could not be said of aging and SD, where a similar subset of genes is changed, but in partially divergent directions. Finally, this work identifies presynaptic vesicular release and intercellular adhesion molecular signatures as novel targets for future SD-countering therapeutics.
2012-07-17 | GSE34424 | GEO
Project description:Sleep deprivation (SD) in young adults is associated with metabolic, stress and cognitive responses that are also characteristic of brain aging. Given that sleep architecture changes with age, including increased fragmentation and decreased slow wave activity, it seems reasonable to investigate potential molecular relationships between SD and aging in brain tissue. Here, we tested the hypothesis that young rats exposed to 24 or 72 hour SD would respond with stress and aging-like shifts in brain hippocampal CA1 gene expression. SD animals showed blood corticosterone and weight changes consistent with a stress response. Microarray results, validated by Western blot and comparison to prior SD studies, pointed to disruptions in neurotransmission, sleep pressure signaling, and macromolecular synthesis. In a separate experiment, animals exposed to 24 or 72 hour novel environment stress recapitulated nearly one third of the SD transcriptional profile, particularly upregulated apoptotic and immune signaling pathways. Compared to aging (based on three previously published independent hippocampal aging studies), SD transcriptional profiles agreed for neurogenesis and energy pathways. However, immune signaling, glial activity, macromolecular synthesis and neuronal function all showed an SD profile that was, at least in part, opposed by aging. We conclude that while stress and SD have discrete molecular signatures, they do show a subset of highly similar changes. However, the same could not be said of aging and SD, where a similar subset of genes is changed, but in partially divergent directions. Finally, this work identifies presynaptic vesicular release and intercellular adhesion molecular signatures as novel targets for future SD-countering therapeutics. Subjects: Male Fischer 344 rats (3-5 months old, Harlan, Indianapolis): 37 in cohort 1 and 32 in cohort 2. Subjects were assigned to one of 5 treatment groups: Home Cage-HC n =17; 24 hour sleep deprivation- 24SD n = 16; 72 hour sleep deprivation- 72SD n = 20; 24 hour novel environment stress- 24NES n = 10; 72 hour novel environment stress- 72NES n = 6. Cohorts 1 and 2 were combined for microarray analyses. Sleep Deprivation: The multiple platform modification (Coenen and van Luijtelaar, 1985) of the classic 'flower pot' (Mendelson et al., 1974) technique in which animals are placed on an elevated platform over water was used. Pairs of SD animals (cage mates) were sleep deprived for 24 or 72 hours. Novel Environment Stress (NES): NES animals were exposed to a novel environment, but were not constrained from sleeping. These NES animals paralleled the sleep deprivation exposure duration (24 hour- n = 10, and 72 hour- n = 6). Tissue Isolation: On the day that animals were removed from the SD chambers, they were anesthetized with CO2 gas and decapitated. Brains were removed and immediately placed in oxygenated artificial cerebrospinal fluid (aCSF) containing (in mM) 114NaCl, 2.5 KCl, 2MgCl2, 30 NaHCO3, 10 Glucose and 2.2CaCl2. Hippocampi were dissected as described previously (Blalock et al., 2003; Kadish et al., 2009). Briefly, dissected hippocampi were immersed in 0C oxygenated aCSF and placed on a chilled glass petri dish. The CA1 region was dissected along the long axis of the hippocampus. CA1 tissue was flash frozen and stored at -80C until further use. Microarray Protocol: GCOS quality control measures of background signal (74.9 ± 2.1 cohort 1; 59.8 ± 2.3 cohort 2) and RawQ (2.3 ± 0.1 cohort 1; 1.9 ± 0.1 cohort 2), as well as a chip x chip correlation matrix of signal intensity data pointed to a global decrease in background signal intensity in Cohort 2. To control for this, each gene expression values for HC, 24SD and 72SD was standardized separately within cohort 1 and cohort 2, and then the two cohorts were combined. This retained the variability of each cohort, but removed the 'cohort effect' from the data. Pre-statistical filtering retained 'A' grade probe sets that were uniquely annotated (Affymetrix, June 2011) with gene symbols and had at least 6 presence calls across all 71 chips. This criterion was selected based on factorial analysis demonstrating < 5% probability of 6 or more chips being rated present for a given probe set by chance (Blalock, unpublished observations).
2012-07-16 | E-GEOD-34424 | biostudies-arrayexpress
Project description:Calorie restriction (CR) enhances longevity and mitigates aging phenotypes in numerous species. Physiological responses to CR are cell-type specific and variable throughout the lifespan; however, the mosaic of molecular changes responsible CR benefits remain unclear, particularly in brain regions susceptible to deterioration throughout aging. Thus, we examined the influence of long-term CR on the CA1 hippocampal region, a key learning and memory brain area that is vulnerable to age-related pathologies, such as Alzheimerâs disease (AD). Through mRNA sequencing and NanoString nCounter analysis, we demonstrate that one year of CR feeding suppresses an age-dependent signature of 882 genes functionally associated with synaptic transmission-related pathways, including calcium signaling, long-term potentiation (LTP), and Creb signaling in wild-type mice. By comparing the influence of CR on hippocampal CA1 region transcriptional profiles at younger- (5 months) and older-adult (15 months) timepoints, we identify conserved upregulation of proteome quality control and calcium buffering genes, including heat shock 70 kDa proteins 1b and 5 (Hspa1b and Hspa5), protein disulfide isomerase family A members 4 and 6 (Pdia4 and Pdia6), and calreticulin (Calr). Expression levels of putative neuroprotective factors, klotho (Kl) and transthyretin (Ttr), are also elevated by CR throughout adulthood, although the global CR-specific expression profiles at young and older timepoints are highly divergent. At a previously unachieved resolution, our results demonstrate conserved activation of neuroprotective gene signatures and broad CR-suppression of age-dependent hippocampal CA1 region expression changes, indicating that CR functionally maintains a more youthful transcriptional state within hippocampal CA1 throughout aging. Hippocampal CA1 region mRNA profiles of younger- (5 months) and older-adult (15 months) mice on calorie-restricted (CR) and normal (AD) diets were generated by deep sequencing using Illumina HiSeq 2500.
2015-07-14 | E-GEOD-69952 | biostudies-arrayexpress
Project description:The project examined age-related change in hippocampal gene expression in Fisher 344 x Brown Norway F1 rats from the NIA aging colony (Adult = 12M, Aged = 24M). CA1, CA3, and DG specific dissections were examined from one cohort of animals and from a second cohort whole hippocampus was used. Hippocampal gene expression with aging in a rat model was examined between Adult (12M) and Aged animals (24M)
2014-04-01 | E-GEOD-55352 | biostudies-arrayexpress
Project description:The present study has used whole-rat genome microarray expression profiling to identify genes whose expression is significantly altered in hippocampal neuronal cultures submitted to oxygen and glucose deprivation (OGD), an established in vitro model for cerebral global ischemia that is suitable for investigations at the molecular level. To do so, total RNA was extracted from hippocampal neuronal cultures at an early (7h) and delayed (24h) time point after OGD, as well as from control neurons. Analysis of gene ontology showed that OGD followed by 7h or 24h of recovery induces changes in the expression levels of genes related with inflammation, response to oxidative stress, metabolism, apoptosis, synaptic proteins and ion channels and, importantly, genes that show different expression levels are mainly specific to one of the two time points of recovery analyzed. The expression levels of several genes were confirmed by qPCR and were in good agreement with the microarray data, showing that the combined use of the OGD model and the microarray technology can be a useful tool for the study molecular mechanisms contributing to the neuronal demise after transient global ischemia. Ischemia induced gene expression in primary hippocampal neuronal rat cultures was measured at 7 and 24 hours after exposure to Oxygen and Glucose deprivation (OGD). Three independent experiments were performed at each time (7 or 24 hours) as independent biological replicates.
2014-06-16 | E-GEOD-54037 | biostudies-arrayexpress
Project description:Calorie restriction (CR) enhances longevity and mitigates aging phenotypes in numerous species. Physiological responses to CR are cell-type specific and variable throughout the lifespan; however, the mosaic of molecular changes responsible CR benefits remain unclear, particularly in brain regions susceptible to deterioration throughout aging. Thus, we examined the influence of long-term CR on the CA1 hippocampal region, a key learning and memory brain area that is vulnerable to age-related pathologies, such as Alzheimer’s disease (AD). Through mRNA sequencing and NanoString nCounter analysis, we demonstrate that one year of CR feeding suppresses an age-dependent signature of 882 genes functionally associated with synaptic transmission-related pathways, including calcium signaling, long-term potentiation (LTP), and Creb signaling in wild-type mice. By comparing the influence of CR on hippocampal CA1 region transcriptional profiles at younger- (5 months) and older-adult (15 months) timepoints, we identify conserved upregulation of proteome quality control and calcium buffering genes, including heat shock 70 kDa proteins 1b and 5 (Hspa1b and Hspa5), protein disulfide isomerase family A members 4 and 6 (Pdia4 and Pdia6), and calreticulin (Calr). Expression levels of putative neuroprotective factors, klotho (Kl) and transthyretin (Ttr), are also elevated by CR throughout adulthood, although the global CR-specific expression profiles at young and older timepoints are highly divergent. At a previously unachieved resolution, our results demonstrate conserved activation of neuroprotective gene signatures and broad CR-suppression of age-dependent hippocampal CA1 region expression changes, indicating that CR functionally maintains a more youthful transcriptional state within hippocampal CA1 throughout aging.
2015-07-14 | GSE69952 | GEO
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
Project description:Aging is under genetic control in C. elegans but the mechanisms of lifespan regulation are not completely known. MicroRNAs (miRNAs) regulate various aspects of development and metabolism and one miRNA has been previously implicated in lifespan. Here we show that multiple miRNAs change expression in C. elegans aging, including novel miRNAs, and that mutations in several of the most up-regulated miRNAs lead to lifespan defects. Some act to promote normal lifespan and stress resistance while others inhibit these phenomena. We find that these miRNAs genetically interact with genes in the DNA damage checkpoint response pathway and in the insulin signaling pathway. Our findings reveal that miRNAs both positively and negatively influence lifespan. Since several miRNAs up-regulated during aging regulate genes in conserved pathways of aging and thereby influence lifespan in C. elegans, we propose that miRNAs may play important roles in stress response and aging of more complex organisms.
2011-01-01 | GSE24510 | GEO