Sleep Deprivation Impairs Vascular Function through Reduced Endothelial Oxidant Stress Clearance in Women
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PROVIDER: PRJNA721094 | ENA |
REPOSITORIES: ENA
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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: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: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 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: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:Study Objectives: Sleep deprivation is highly prevalent and caused by conditions such as night shift work or illnesses like obstructive sleep apnea. Compromised sleep is proposed to play a role in several cardiovascular, immune related and neurodegenerative disorders. We recently published human serum proteome changes after a simulated night shift. This study aimed to further explore changes in the human blood serum after 6h of sleep deprivation at night by proteomics and systems biological databases. Methods: Human blood serum samples from 8 self-declared healthy females were analyzed using mass spectrometry and high-pressure liquid chromatography. Each subject was their own control, and two samples were taken from each subject, the first one after 6h of sleep at night and the second one after 6h of sleep deprivation the following night. Biological databases and bioinformatic software were used for systems biological analyzes and comparative analysis with other published sleep-related datasets. Results: Of 494 proteins, 66 were found to be differentially expressed after 6h of sleep deprivation at night. Functional enrichment analysis revealed associations of these proteins with several biological functions related to the regulation of cellular processes like protein- and ion-binding connected to platelet degranulation and blood coagulation, as well as associations with different curated gene sets. Conclusions: This study presents serum proteomic changes after 6h of sleep deprivation, supports previous findings that only 6h of sleep deprivation affects several biological processes and revealed a molecular signature of protein changes related to pathological conditions like altered coagulation and platelet function, impaired lipid and immune function and cancer. Keywords: Human blood serum, proteomics, sleep deprivation, cellular stress, functional enrichment analysis
2024-06-27 | PXD045729 | Pride
Project description:Sleep is deeply involved in neuroimmune regulation, while the mechanism is yet to be elucidated. Experimental manipulation of sleep duration provides a reliable measure for evaluating how sleep regulates innate immunity. Here we report a modified sleep deprivation paradigm (SD) that can constantly awaken the mice with more than 95% efficiency, and investigate the effects of prolonged sleep deprivation on mice's immune systems.
2023-11-27 | GSE213497 | GEO