Small intestinal crypt cell subsets and gene expression in sleep-deprived mice
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE289089 | GEO | 2025/12/30
REPOSITORIES: GEO
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Project description:Small intestinal crypt cell subsets and gene expression in sleep-deprived mice
| PRJNA1221288 | ENA
Project description:Sleep is an evolutionarily conserved physiological process implicated in the consolidation of learning and memory. In our study, sleep deprivation-induced cognitive deficits in zebrafish are mediated through reduction in glucose metabolism to the hexosamine biosynthetic pathway. Therefore, we perform the microarray to confirm glucose metabolic pathway- and nerve system-related genes expression using mRNA from brains of control, sleep-deprived and fear-conditioned zebrafish groups.
2019-03-14 | GSE128217 | 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:Analysis of brain of Canton-S females deprived of sleep by perturbations during their normal sleep period. Perturbation effect also assessed during their active period to control for its effect during sleep deprivation. Results suggest processes altered during prolonged wakefulness and during sleep.
2007-07-06 | E-GEOD-4174 | 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:Study objectives: Acute sleep deprivation affects both central and peripheral biological processes. Prior research has mainly focused on specific proteins or biological pathways that are dysregulated in the setting of sustained wakefulness. This pilotexploratory study’s objective wasaimed to provide a comprehensive view of the biological processes and proteins impacted by acute sleep deprivation in both plasma and cerebrospinal fluid (CSF). Methods: We collected plasma and CSF from human participants during one night of sleep deprivation and control normal sleep conditions. 1300 proteins were measured at hour 0 and hour 24 using a high-scale aptamer-based proteomics platform (SOMAomascan) and a systematics biological database tool (Metascape) was used to reveal dysregulated biological pathways. Results: Acute sleep deprivation lead to opposite effects in plasma and CSF, decreasingdecreased the number of upregulated and downregulated differential protein expression and biological pathways and proteins in plasma but increased upregulated and downregulated protein and biological pathwayssing them in CSF. Predominantly affected pProteins and n pathways were associated with that were predominantly affected by sleep deprivation included immune response, inflammation, phosphorylation, membrane signaling, cell-cell adhesion, and extracellular matrix organization. Conclusions: The identified modification across biofluids adds to evidence that acute sleep deprivation has important impacts on biological pathways and proteins that can negatively affect human health. As a hypothesis-driving study, these findings may help with the exploration of novel mechanisms that mediate sleep loss and associated conditions, drive the discovery of new sleep loss biomarkers, and ultimately aid in the identification of new targets for intervention to human diseases.
2023-12-14 | GSE244817 | GEO
Project description:To gain insight into the molecular changes of sleep need, this study addresses gene expression changes in a subpopulation of neurons selectively activated by sleep deprivation. Whole brain expression analyses after 6h sleep deprivation clearly indicate that Homer1a is the best index of sleep need, consistently in all mouse strains analyzed. Transgenic mice expressing a FLAG-tagged poly(A)-binding protein (PABP) under the control of Homer1a promoter were generated. Because PABP binds the poly(A) tails of mRNA, affinity purification of FLAG-tagged PABP proteins from whole brain lysates, is expected to co-precipitate all mRNAs from neurons expressing Homer1a. Three other activity-induced genes (Ptgs2, Jph3, and Nptx2) were identified by this technique to be over-expressed after sleep loss. All four genes play a role in recovery from glutamate-induced neuronal hyperactivity. The consistent activation of Homer1a suggests a role for sleep in intracellular calcium homeostasis for protecting and recovering from the neuronal activation imposed by wakefulness. Experiment Overall Design: Experiments were performed on male mice, 12 weeks of age +/- 1 week. Animals were housed in polycarbonate cages (31x18x18cm) in an experimental room with an ambient temperature varying from 23° to 25°C under a 12:12 hrs light/dark cycle. Food and water were available ad libitum. At light onset mice were either sleep deprived by gentle handling (n=10) or left undisturbed (n=10) for 6 hrs. Animals were then randomly sacrificed by cervical dislocation. Total RNA from the whole brain was isolated for control (n=4) and sleep deprived (n=4) using a commercial RNA extraction kit (RNeasy Lipid Tissue Kit, Quiagen). Specific Homer1a-expressing cells polyA RNAs were immunoprecipitated following the total brain crosslinking (1% formaldehyde perfusion) for sleep deprived (n=6) and control (n=6) animals. The total RNA from the pull-down supernatants were also harvested (n=4). To test for transcriptional changes after sleep deprivation Homer1a-expressing cells, we proceeded in 2 steps: (1) identify probe sets enriched in the pull-down extracts, (2) among those probe sets compare sleep deprivation to control condition in both pull-down (6 vs. 6 chip comparison) and whole-brain (4 vs. 4 chip comparison) extracts. 4728 probe sets were significantly enriched at 5% FDR when pull-downs were compared to both supernatant and whole-brain extracts.
2008-06-16 | E-GEOD-9443 | biostudies-arrayexpress
Project description:Extended periods of waking result in physiological impairments in humans, rats, and flies. Sleep homeostasis, the increase in sleep observed following sleep loss, is believed to counter the negative effects of prolonged waking by restoring vital biological processes that are degraded during sleep deprivation. Sleep homeostasis, as with other behaviors, is influenced by both genes and environment. We report here that during periods of starvation, flies remain spontaneously awake but, in contrast to sleep deprivation, do not accrue any of the negative consequences of prolonged waking. Specifically, the homeostatic response and learning impairments that are a characteristic of sleep loss are not observed following prolonged waking induced by starvation. To identify the genes responsible for the protective effects of starvation we conducted transcription profiling of sleep deprived flies that accrue sleep debt compared to starved siblings that do not. Genes involved in lipid metabolism were highly enriched in our dataset of 84 differentially regulated transcripts. Follow up genetic studies established that 6 genes involved in lipid metabolism strongly influence sleep homeostasis. Two of these genes, brummer (bmm) and Lipid storage droplet 2 (Lsd2), are in the same lipolysis pathway but exert antagonistic effects on lipid storage. bmm mutant flies have excess fat stores and display a large homeostatic response following sleep deprivation. In contrast, Lsd2 mutant flies, which phenocopy aspects of starvation as measured by low triglyceride stores, do not exhibit a homeostatic response following sleep loss. Importantly, Lsd2 mutant flies are not learning impaired after sleep deprivation. These results provide the first genetic evidence, to our knowledge, that lipid metabolism plays an important role in regulating the homeostatic response and can protect against neuronal impairments induced by prolonged waking. Two-condition experiments: sleep deprived vs starved. RNA from 8 biological replicates for each condition was pooled in groups of 2 to create 4 samples. Each of the 4 samples is run in duplicate with untreated circadian matched controls.
2014-04-15 | E-GEOD-18550 | biostudies-arrayexpress
Project description:Sleep regulation follows a homeostatic pattern. The mammalian cerebral cortex is the repository of homeostatic sleep drive and neurons and astrocytes of the cortex are principal responders of sleep need. The molecular mechanisms by which these two cell types respond to sleep loss are not yet clearly understood. By combining cell-type specific transcriptomics and nuclear proteomics we investigated how sleep loss affects the cellular composition and molecular profiles of these two cell types in a focused approach. The results indicate that sleep deprivation regulates gene expression and nuclear protein abundance in a cell-type-specific manner. Our integrated multi-omics analysis suggests that this distinction arises because neurons and astrocytes employ different gene regulatory strategies under accumulated sleep pressure. These findings provide a comprehensive view of the effects of sleep deprivation on gene regulation in neurons and astrocytes.
2025-05-30 | PXD055214 | Pride
Project description:Although at the organismal level sleep is defined as a behavioral state, at the level of the cerebral cortex sleep has a distinct local and use-dependent aspect. This observation raises the question whether sleep is a functional property of a complex brain or occurs at the level of neuronal assemblies with populations that were active more during wakefulness needing more intense sleep to recover. Here we show that primary cortical cultures have the capacity to change between sleep- and wake-like states that share key signatures with their in vivo counterparts. Cortical cultures initially exhibit random firing activity that is gradually replaced by a M-bM-^@M-^\sleep-likeM-bM-^@M-^] synchronized burst-pause firing activity as neurons mature and make connections. When stimulated with excitatory neurotransmitters, transient tonic firing is observed, followed by the reappearance of a M-bM-^@M-^\sleep-likeM-bM-^@M-^] state. Besides electrophysiological similarities also the transcriptional profile of stimulated cortical cultures greatly resembles that of the cortex of sleep deprived animals. We then used our in vitro model to map the metabolic pathways activated by the M-bM-^@M-^\wake-likeM-bM-^@M-^] state and found evidence for increased lysolipid release, strongly suggesting that sleep plays a role in neuronal membrane homeostasis. With our in vitro model the cellular and molecular consequences of sleep loss and the genetic determinants of disturbed sleep can now be investigated in a dish. Keywords: stress response For the in vivo transcriptome analyses mice were sleep deprived for 6 hours and brain harvested immediately afterwards. For the in vitro analyses, cortical cultures were stimulated with a neurotransmitter cocktail and cells harvested 3 hours afterwards. Control mice were kept undisturbed in their home cage and control cultures were sham stimulated with water. Also, another set of sleep deprived mice as well as stimulated cultures were allowed to recover before being sampled the next day at the time of day at which sleep deprivation or stimulation started the day before).
2012-08-31 | E-GEOD-33491 | biostudies-arrayexpress