Ontology highlight
ABSTRACT:
PROVIDER: PRJNA889049 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR21854712_1.fastq.gz | Fastqsanger.gz | |||
| SRR21854712_2.fastq.gz | Fastqsanger.gz | |||
| SRR21854713_1.fastq.gz | Fastqsanger.gz | |||
| SRR21854713_2.fastq.gz | Fastqsanger.gz | |||
| SRR21854714_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 18 |
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Project description:Sleep supports lifelong brain health and cognition. Sleep loss in early life can drive lasting changes in adult behavior, indicating sleep plays a distinct but poorly understood role supporting brain development. We systematically examined the molecular and behavioral adaptations and synaptic consequences of acute sleep deprivation (SD) in developing and adult mice. Developing mice lack robust adaptations to SD, exacerbating cognitive deficits. Synapse proteome and phosphoproteome analysis revealed profound vulnerability to SD in developing mice, including immediate impacts on synaptogenesis and key aspects of brain development. With maturation, a unified biochemical effect of sleep on synapses emerges, together with robust adaptations and resilience to SD. Our findings show sleep plays a distinct role in early life supporting synapse development, transitioning to homeostatic functions with maturation.
2024-10-08 | PXD047381 | Pride
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:Impaired sleep is a common aspect of aging and often precedes the onset of Alzheimer's disease. Here, we compare the effects of sleep deprivation in young wild-type mice and their APP/PS1 littermates, a murine model of Alzheimer's disease. After 7 h of sleep deprivation, both genotypes exhibit an increase in EEG slow-wave activity. However, only the wild-type mice demonstrate an increase in the power of infraslow norepinephrine oscillations, which are characteristic of healthy non-rapid eye movement sleep. Notably, the APP/PS1 mice fail to enhance norepinephrine oscillations 24 h after sleep deprivation, coinciding with an accumulation of cerebral amyloid-β protein. Proteome analysis of cerebrospinal fluid and extracellular fluid further supports these findings by showing altered protein clearance in APP/PS1 mice. We propose that the suppression of infraslow norepinephrine oscillations following sleep deprivation contributes to increased vulnerability to sleep loss and heightens the risk of developing amyloid pathology in early stages of Alzheimer's disease.
2025-01-30 | PXD054763 | Pride
Project description:Molecular profiles in sleep and sleep deprivation in peripheral tissues using microarrays Time point study. Mice were sacrificed by cervical dislocaton following 3, 6, 9, and 12 h of total sleep deprivation (n = 8 or 9 at each time point). Deprivation was initiated at lights-on and performed through gentle handling.
2012-11-17 | E-GEOD-42324 | biostudies-arrayexpress
Project description:Molecular profiles in sleep and sleep deprivation in peripheral tissues using microarrays Time point study. Mice were sacrificed by cervical dislocaton following 3, 6, 9, and 12 h of total sleep deprivation (n = 8 or 9 at each time point). Deprivation was initiated at lights-on and performed through gentle handling.
2012-11-17 | E-GEOD-42323 | biostudies-arrayexpress
Project description:Sleep abnormalities are common with aging. Studies show that sleep plays important roles in brain functions, and loss of sleep is associated with increased risks for neurological diseases. In this study, we used next generation RNA-sequencing to explore effects of age on transcriptome changes between sleep and sleep deprivation in medial prefrontal cortex. Old mice showed a 30% reduction in the number of genes significantly altered between sleep/wake, and, in general, had smaller magnitudes of changes in differentially expressed genes compared to young. Gene ontology analysis revealed differential age-effects on certain pathways. Compared to young mice, many of the wake-active functions were similarly induced by sleep deprivation in old mice, whereas many of the sleep-active pathways were attenuated in old mice. We found similar magnitude of changes in a number of synaptic homeostasis genes (Fos, Arc, and Bdnf) induced by sleep deprivation, suggesting intact synaptic upscaling during extended wakefulness with aging. However, sleep-activated processes, such as DNA repair, synaptogenesis, and axon guidance, were sensitive to the effect of aging. Old mice expressed elevated levels of immune-related genes when compared to young mice, and enrichment analysis using cell-type specific markers indicated up-regulation of microglia and oligodendrocyte genes in old mice. Moreover, gene sets of the two cell types showed age-specific sleep/wake regulation. This study indicates alteration of molecular changes with sleep in old mice.
2020-01-03 | GSE128770 | GEO
Project description:Qutantitative proteomic/phosphoproteomic studies of prolonged sleep deprivation mice models.
2022-06-02 | MSV000089587 | MassIVE
Project description:To assess the effect of sleep deprivation on glucose metabolism and elucidate the mechanism, we established the mouse model wth C57BL/6J that is useful for the intervention on sleep deprivation associated diabetes and evaluate the liver metabolism and gene expression. Single six hours sleep deprivation induced increased hepatic glucose production assessed by pyruvate tolerance test and the hepatic triglyceride content was significantly higher in the sleep deprivation group than freely sleeping control group. Liver metabolites such as ketone bodies were increased in sleep deprivation group. Some gene expressions which associated with lipogenesis were increased.
2016-12-27 | GSE92913 | GEO
Project description:Introduction: Sleep deprivation is associated with increased cardiovascular risk, which is more pronounced in women than men; however, causal evidence is lacking and the underlying mechanisms are unclear. We used randomized crossover design of prolonged sleep deprivation that mimics “life-like conditions” and endothelial cells (ECs) harvested from healthy women to investigate directly whether sleep deprivation impairs endothelial function and to identify underlying mechanisms. Methods: Healthy women with normal habitual sleep (7-9 h/day) were randomly allocated to 6-weeks of adequate sleep (7-9 h/day) or sleep deprivation (1.5 h less than habitual sleep) in a crossover design. Sleep duration was monitored objectively by actigraphy. EC harvesting and brachial artery flow-mediated dilation (FMD) were performed at baseline and the end of adequate sleep and sleep deprivation period. Results: Twenty-eight healthy women (mean [SE] age 35±13 years; BMI 25±3 kg/m2) participated. Compared with adequate sleep, sleep deprivation reduced FMD (mean±SE 8.65±0.48 vs. 7.35±0.39, p=0.02) and increased EC inflammation (nuclear factor-κB nuclear fluorescence area mean±SE 1.36±0.24 vs. 2.04±0.38 μm2, p=0.03 and mRNA expression of vascular cell adhesion molecule-1 mean±SE 1.00±0.19 vs. 2.31±0.72, p=0.04) compared with adequate sleep. Sleep deprivation increased EC oxidative stress by 67% compared with adequate sleep (redox sensitive fluorogenic probe fluorescence intensity, p=0.002) without upregulating antioxidant response. Using RNA-seq and a predicted protein-protein interaction algorithm, we identified reduced expression of serum response factor, a transcription factor that primes cortical response to sleep deprivation, and its endothelial target Defective in Cullin Neddylation-1 Domain Containing 3 as novel mediators of impaired nuclear factor (erythroid-derived 2)-like 2-mediated antioxidant responses in ECs in sleep deprivation. Conclusion: Sleep deprivation impairs clearance of endothelial oxidant stress accumulated during wakefulness leading to endothelial dysfunction and potentially increased cardiovascular risk in women. Trial Registration Number: ClinicalTrials.gov NCT02835261
2024-04-05 | GSE171831 | 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. Keywords: sleep deprivation, neuronal subpopulation transcriptome
2007-12-07 | GSE9443 | GEO