Sleep deprivation disturbs diurnal rhythmicity of gut microbiota and inflammatory responses in mice
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PROVIDER: PRJEB95809 | ENA |
REPOSITORIES: ENA
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Project description:To address whether changes in gene expression in blood cells with sleep loss are different in individuals resistant and sensitive to sleep deprivation (SD). Blood draws every 4 hours during a 3-day study: 24-hour normal baseline, 38 hours of continuous wakefulness and subsequent recovery sleep, for a total of 19 time-points per subject, with every 2-hr psychomotor vigilance test (PVT) assessment when awake. Fourteen subjects who were previously identified as behaviourally resistant (n=7) or sensitive (n=7) to SD by PVT. Intervention consisted of 38 hours continuous wakefulness. We found 4,481 unique genes with a significant 24-hour diurnal rhythm during a normal sleep-wake cycle in blood (false discovery rate [FDR] <5%). Biological pathways were enriched for biosynthetic processes during sleep. After accounting for circadian effects, two genes (SREBF1 and CPT1A, both involved in lipid metabolism) exhibited small, but significant, linear changes in expression with the duration of SD (FDR<5%). The main change with SD was a reduction in the amplitude of the diurnal rhythm of expression of normally cycling probe sets. This reduction was noticeably higher in behaviourally resistant subjects than sensitive subjects, at any given p-value. Furthermore, blood cell type enrichment analysis showed that the expression pattern difference between sensitive and resistant subjects is mainly found in cells of myeloid origin, such as monocytes. Individual differences in behavioural effects of sleep deprivation are associated with differences in diurnal amplitude of gene expression for genes that show circadian rhythmicity.
2014-10-02 | GSE56931 | GEO
Project description:To address whether changes in gene expression in blood cells with sleep loss are different in individuals resistant and sensitive to sleep deprivation (SD). Blood draws every 4 hours during a 3-day study: 24-hour normal baseline, 38 hours of continuous wakefulness and subsequent recovery sleep, for a total of 19 time-points per subject, with every 2-hr psychomotor vigilance test (PVT) assessment when awake. Fourteen subjects who were previously identified as behaviourally resistant (n=7) or sensitive (n=7) to SD by PVT. Intervention consisted of 38 hours continuous wakefulness. We found 4,481 unique genes with a significant 24-hour diurnal rhythm during a normal sleep-wake cycle in blood (false discovery rate [FDR] <5%). Biological pathways were enriched for biosynthetic processes during sleep. After accounting for circadian effects, two genes (SREBF1 and CPT1A, both involved in lipid metabolism) exhibited small, but significant, linear changes in expression with the duration of SD (FDR<5%). The main change with SD was a reduction in the amplitude of the diurnal rhythm of expression of normally cycling probe sets. This reduction was noticeably higher in behaviourally resistant subjects than sensitive subjects, at any given p-value. Furthermore, blood cell type enrichment analysis showed that the expression pattern difference between sensitive and resistant subjects is mainly found in cells of myeloid origin, such as monocytes. Individual differences in behavioural effects of sleep deprivation are associated with differences in diurnal amplitude of gene expression for genes that show circadian rhythmicity. Blood draws were done every 4 hours during a 3-day (+1 baseline day) study: 24-hour normal baseline (6 time points: day 1 8hr, 12hr, 16hr, 20hr, day 2 0hr, 4hr), 38 hours of continuous wakefulness (10 time points: day 2 8hr, 12hr, 16hr, 20hr, day 3 0hr, 4hr, 8hr, 12hr, 16hr, 20hr) and subsequent recovery sleep (3 time points: day 4 0hr, 4hr, 8hr), for a total of 19 time-points per subject, with every 2-hr psychomotor vigilance test (PVT) assessment when awake. The missing/failed samples were as following: Resistant subjects (total 10 samples): BH006 day 2 20hr, 12hr, BH003 day 2 12hr, 4hr, BH003 day 3 4hr, BH008 day 4 0hr, BH008 day 1 16hr, BH008 day 3 16hr 20hr, BH010 day 4 0hr; Sensitive subjects (total 7 samples): BH004 day 2 12hr and 1 more missing sample, BH026 day 2 4hr, BH007 day 2 20hr and 1 more missing sample, BH016 day 2 4hr, BH015 day 3 0hr.
2014-10-02 | E-GEOD-56931 | biostudies-arrayexpress
Project description:Inadequate sleep prevails in modern society and it impairs the circadian transcriptome. However, whether acute sleep deprivation has impact on the circadian rhythms is not clear. Here, we show that in mouse lung, a 10-hour acute sleep deprivation can alter the circadian expression of approximally 3,000 genes. We found that circadian rhythm disappears in genes related to metabolism and signaling pathways regulating protein phosphorylation after acute sleep deprivation, while the core circadian regulators do not change much in rhythmicity. Importantly, the strong positive correlation between mean expression and amplitude (E-A correlation) of cycling genes has been validated in both control and sleep deprivation conditions, supporting the energetic cost optimization model of circadian gene expression. Thus, we reveal that acute sleep deprivation leads to a profound change in the circadian gene transcription that influences the biological functions in lung.
2021-02-09 | GSE166335 | GEO
Project description:Purpose: To determine the specific effects of 6 hours sleep deprivation after a learning event on the transcriptomes of microglia. Sleep deprivation can generate inflammatory responses in the neuronal environment. In turn, this inflammation increases sleep drive, leading to a rebound in sleep duration. Microglia, a type of support cell found exclusively in the brain, have previously been found to release of inflammatory signals and exhibit altered characteristics in response to sleep deprivation. Together, this suggests microglia may be partially responsible for the brain’s response to sleep deprivation through their inflammatory activity. In this study, we fully and selectively ablated microglia from the mouse brain and assessed resulting sleep, circadian, and sleep deprivation phenotypes. We find microglia are dispensable for both homeostatic sleep and circadian function and the sleep rebound response to sleep deprivation. However, we uncover a phenomenon by which microglia appear to be essential for the protection of synapses and associated memories formed during a period of sleep deprivation, further expanding the list of known functions for microglia in synaptic modulation.
2021-05-12 | GSE174231 | GEO
Project description:Purpose: To comprehensively identify the gene expression changes that occur after acute sleep deprivation. Method: We performed total RNA sequencing after 5hours of sleep deprivation. Results: Using total RNA-sequencing, we show that acute sleep deprivation causes dramatic gene expression changes in the mouse hippocampus. Conclusion: This study provides insight into the biological impact of acute sleep deprivation.
2021-03-01 | GSE166831 | GEO
Project description:Analysis of the effects of sleep deprivation, recovery sleep, and three time-of-day controls on seven brain regions laser microdissected from mouse brain. The regions include the locus coeruleus, suprachiasmatic nucleus, hypocretin area, tuberomammillary nucleus, orbital cortex, posteromedial cortical amygdala, and entorhinal cortex. In this study, 7 brain regions were collected by laser microdissection from brain tissue of mice from 5 different treatment groups and used for microarray experiments. Four biological replicates were generated for each regionxcondition. Conditions are: SD, sleep deprivation for 6 hours from ZT0 - 6; SDC, time-of-day control for SD at ZT6; RS, recovery sleep for 4 hours following SD; RSC, time-of-day control for RS at ZT10; W, spontaneous waking at ZT18.
2010-08-16 | E-GEOD-23628 | biostudies-arrayexpress
Project description:Sleep loss regulates gene expression throughout the brain and impacts learning and memory. However, the molecular consequences of sleep deprivation and the ability of subsequent sleep (recovery sleep) to restore baseline gene expression remain underexplored. Our goal here is to overview transcriptional changes at the gene level in the cortex of adult male wildtype mice in response to sleep loss and recovery sleep. This dataset constitutes an integration of novel data with two publicly available RNA-seq studies and contains 3, 5, and 6 hours of sleep deprivation and 2 and 6 hours of recovery sleep time points.
2024-08-19 | GSE237419 | GEO
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:GABAergic transmission controls cortical sleep, however the molecular determinants of GABAergic control of this phenomenon are unknown. We used immunoprecipitation of the inhibitory postsynaptic protein gephyrin to identify gephyrin interactors at ZT6 (sleep) and ZT6 with sleep deprivation (ZT6SD).
2024-07-25 | PXD048929 | Pride
Project description:To gain insight into the dynamic molecular processes that are altered during prolonged wakefulness and during sleep. We performed an RNA expression profiling study examining temporal changes in the brain of Drosophila in relationship to the duration of prior sleep or wakefulness. Our experimental design allowed us to determine whether genes identified as differentially regulated between sleep and wakefulness were up- or down-regulated in these states. Because stimulation of the experimental animal during the normal sleep period is used to prolong wakefulness in most experimental paradigms, the interpretation of the effects of prolonged wakefulness is confounded by the effect of the perturbation stimulus itself on the animal’s biology. We controlled for this effect in our experimental paradigm by examining gene expression changes in response to identical stimulation but during the animal’s normal wakefulness. The design of our study also allowed us to control for circadian variation in gene expression, since we compared sleeping and sleep deprived flies at the same diurnal time. Keywords: sleep deprivation, time course, stress response
2006-02-27 | GSE4174 | GEO