Disruption of Circadian Transcriptome in Lung by Acute Sleep Deprivation
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE166335 | GEO | 2021/02/09
REPOSITORIES: GEO
Similar Datasets
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:<p>Sleep is essential for life. A good night's sleep is pleasurable and sleep deprivation is stressful. Prolonged sleep loss impairs temperature control, metabolism, immunity, and ultimately leads to death. Extensive observational and epidemiological evidence indicates that optimal sleep duration of 8 hours is associated with the maintenance of good health. In our society, however, most people only get 6.5 - 7 hours. Suboptimal sleep duration has a strong association with mortality and morbidity. Lack of sleep has been linked to cardiovascular diseases, obesity, hypertension, type 2 diabetes, and other health/cognition conditions. It is clear that the biological need for sleep varies dramatically among humans. Sleep and circadian disorders can include Familial Advanced Sleep Phase (FASP), Delayed Sleep Phase (DSP), Advanced Sleep Phase (ASP), Natural Short Sleepers (NSS) or Long Sleeping. In example, Natural Short Sleepers (NSS) have a lifelong tendency to sleep only 4 - 6 hours per night and to awaken refreshed and energetic. Natural Long Sleepers biologically require 9 - 10 hours/night to feel well rested.</p> <p>The 'Sleep and Circadian Disorders Study' (SACDS) at the University of California San Francisco, set out to investigate the mechanisms involved in regulating sleep duration, patterns and sleep quality regulation by identifying and characterization of individuals and families with unusual sleep and circadian rhythm behavior patterns.</p> <p>SACDS participants were screened with a "General Sleep Questionnaire" that inquired about multiple aspects of sleep, including habitual work-day versus non-work day sleep-wake schedules, permits calculation of subjective habitual initial sleep onset, final sleep offset, and number of awakenings. There was an additional screening process including demographic data, sleep, mood, behavioral and general medical questionnaires, plus the study consent.</p> <p>After the extensive screening of 117 participants, blood samples were collected from 38 individuals and of those 10 samples were chosen for whole exome sequencing analysis.</p>
| phs001270 | dbGaP
Project description:Disruption of Circadian Transcriptome in Lung by Acute Sleep Deprivation
| PRJNA700534 | ENA
Project description:Despite an established link between sleep deprivation and epigenetic processes in humans, it remains unclear to what extent sleep deprivation modulates DNA methylation. We performed a within subject randomized blinded study with 16 healthy subjects to examine the effect of one night of total acute sleep deprivation (TSD) on the genome wide methylation profile in blood compared to normal sleep. Genome-wide differences in methylation between both conditions were assessed by applying a paired regression model that corrected for monocyte subpopulations (neutrophil/leukocyte ratio). Additionally, the correlations between the methylation of genes detected to be modulated by TSD and gene expression were examined in a separate, publicly available cohort of ten healthy male donors (E-GEOD-49065). Sleep deprivation significantly affected the DNA methylation profile both independently and in dependency of shifts in monocyte composition. Our study detected differential methylation of 269 probes. Notably, one CpG site was located 69bp upstream of ING5, which has been shown to be differentially expressed following sleep deprivation. Gene set enrichment analysis detected the Notch and Wnt signaling pathways to be enriched among the differentially methylated genes. These results provide evidence that total acute sleep deprivation alters the methylation profile in healthy human subjects. This is, to our knowledge, the first study that systematically investigated the impact of total acute sleep deprivation on genome-wide DNA methylation profiles in blood and related the epigenomic findings to the expression data.
2016-06-30 | E-MTAB-4664 | biostudies-arrayexpress
Project description:This a model from the article:
Sleep deprivation in a quantitative physiologically based model of the ascending
arousal system.
Phillips AJ, Robinson PA. J Theor Biol
2008 Dec 21;255(4):413-23 18805427
,
Abstract:
A physiologically based quantitative model of the human ascending arousal system
is used to study sleep deprivation after being calibrated on a small set of
experimentally based criteria. The model includes the sleep-wake switch of
mutual inhibition between nuclei which use monoaminergic neuromodulators, and
the ventrolateral preoptic area. The system is driven by the circadian rhythm
and sleep homeostasis. We use a small number of experimentally derived criteria
to calibrate the model for sleep deprivation, then investigate model predictions
for other experiments, demonstrating the scope of application. Calibration gives
an improved parameter set, in which the form of the homeostatic drive is better
constrained, and its weighting relative to the circadian drive is increased.
Within the newly constrained parameter ranges, the model predicts repayment of
sleep debt consistent with experiment in both quantity and distribution,
asymptoting to a maximum repayment for very long deprivations. Recovery is found
to depend on circadian phase, and the model predicts that it is most efficient
to recover during normal sleeping phases of the circadian cycle, in terms of the
amount of recovery sleep required. The form of the homeostatic drive suggests
that periods of wake during recovery from sleep deprivation are phases of
relative recovery, in the sense that the homeostatic drive continues to converge
toward baseline levels. This undermines the concept of sleep debt, and is in
agreement with experimentally restricted recovery protocols. Finally, we compare
our model to the two-process model, and demonstrate the power of physiologically
based modeling by correctly predicting sleep latency times following deprivation
from experimental data.
This model was taken from the CellML repository
and automatically converted to SBML.
The original model was:
Phillips AJ, Robinson PA. (2008) - version=1.0
The original CellML model was created by:
Catherine Lloyd
c.lloyd@auckland.ac.nz
The University of Auckland
This model originates from BioModels Database: A Database of Annotated Published Models (http://www.ebi.ac.uk/biomodels/). It is copyright (c) 2005-2011 The BioModels.net Team.
To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication
for more information.
In summary, you are entitled to use this encoded model in absolutely any manner you deem suitable, verbatim, or with modification, alone or embedded it in a larger context, redistribute it, commercially or not, in a restricted way or not..
To cite BioModels Database, please use: Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novère N, Laibe C (2010) BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. BMC Syst Biol., 4:92.
2005-01-01 | MODEL1006230115 | BioModels
Project description:This a model from the article:
Sleep deprivation in a quantitative physiologically based model of the ascending
arousal system.
Phillips AJ, Robinson PA. J Theor Biol
2008 Dec 21;255(4):413-23 18805427
,
Abstract:
A physiologically based quantitative model of the human ascending arousal system
is used to study sleep deprivation after being calibrated on a small set of
experimentally based criteria. The model includes the sleep-wake switch of
mutual inhibition between nuclei which use monoaminergic neuromodulators, and
the ventrolateral preoptic area. The system is driven by the circadian rhythm
and sleep homeostasis. We use a small number of experimentally derived criteria
to calibrate the model for sleep deprivation, then investigate model predictions
for other experiments, demonstrating the scope of application. Calibration gives
an improved parameter set, in which the form of the homeostatic drive is better
constrained, and its weighting relative to the circadian drive is increased.
Within the newly constrained parameter ranges, the model predicts repayment of
sleep debt consistent with experiment in both quantity and distribution,
asymptoting to a maximum repayment for very long deprivations. Recovery is found
to depend on circadian phase, and the model predicts that it is most efficient
to recover during normal sleeping phases of the circadian cycle, in terms of the
amount of recovery sleep required. The form of the homeostatic drive suggests
that periods of wake during recovery from sleep deprivation are phases of
relative recovery, in the sense that the homeostatic drive continues to converge
toward baseline levels. This undermines the concept of sleep debt, and is in
agreement with experimentally restricted recovery protocols. Finally, we compare
our model to the two-process model, and demonstrate the power of physiologically
based modeling by correctly predicting sleep latency times following deprivation
from experimental data.
This model was taken from the CellML repository
and automatically converted to SBML.
The original model was:
Phillips AJ, Robinson PA. (2008) - version=1.0
The original CellML model was created by:
Catherine Lloyd
c.lloyd@auckland.ac.nz
The University of Auckland
This model originates from BioModels Database: A Database of Annotated Published Models (http://www.ebi.ac.uk/biomodels/). It is copyright (c) 2005-2011 The BioModels.net Team.
To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication
for more information.
In summary, you are entitled to use this encoded model in absolutely any manner you deem suitable, verbatim, or with modification, alone or embedded it in a larger context, redistribute it, commercially or not, in a restricted way or not..
To cite BioModels Database, please use: Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novère N, Laibe C (2010) BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. BMC Syst Biol., 4:92.
2005-01-01 | MODEL1006230110 | BioModels
Project description:The sleep-wake cycle is determined by a circadian and a sleep homeostatic process. However, the molecular impact of these two processes and their interaction on different cell populations in the brain remain unknown. To fill this gap, we have profiled the single-cell transcriptome of adult fruit fly brains across the sleep-wake cycle and different circadian times. We show cell type-specific transcriptomic changes between sleep/wakefulness states, different levels of sleep drive, and varying circadian times, with glial cells displaying the largest variations. Furthermore, the cell types whose transcriptomic dynamics correlate with the sleep homeostat or circadian clock are largely non-overlapping, with the exception of glial cells. Diminishing the circadian clock only in glial cells impairs the homeostatic sleep rebound after sleep deprivation. These findings reveal a comprehensive picture of different effects of sleep homeostatic and circadian processes on different cell types and define glial cells as the interaction sites of these two processes to determine sleep-wake dynamics.
2023-11-29 | GSE221239 | GEO
Project description:The circadian clock drives daily changes of physiology, including sleep-wake cycles, by regulating transcription, protein abundance and function. Circadian phosphorylation controls cellular processes in peripheral organs, but little is known about its role in brain function and synaptic activity. We applied advanced quantitative phosphoproteomics to mouse forebrain synaptoneurosomes isolated across 24h, accurately quantifying almost 8,000 phosphopeptides. Remarkably, half of the synaptic phosphoproteins, including numerous kinases, had large-amplitude rhythms peaking at rest-activity and activity-rest transitions. Bioinformatic analyses revealed global temporal control of synaptic function via phosphorylation, including synaptic transmission, cytoskeleton reorganization and excitatory/inhibitory balance. Remarkably, sleep deprivation abolished 98% of all phosphorylation cycles in synaptoneurosomes, indicating that sleep-wake cycles rather than circadian signals are main drivers of synaptic phosphorylation, responding to both sleep and wake pressures.
2019-10-14 | PXD010697 | Pride