Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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The peripheral genome-wide gene expression profiles in humans after prolonged wakefulness and sleep recovery

ABSTRACT: Although the specific functions of sleep have not been completely elucidated, the literature has suggested that sleep is essential for proper homeostasis. Sleep loss is associated with changes in behavioral, neurochemical, cellular, and metabolic functions as well as impaired immune response. We evaluated the gene expression profiles of healthy volunteers submitted to 48 hours of prolonged wakefulness (PW) followed by 12 hours of sleep recovery (SR) using high-resolution microarrays. Peripheral whole blood was collected in the morning before the initiation of sleep deprivation (baseline), after the second night of PW, and one night after SR. the identified differentially expressed genes were related to immune response, DNA damage and repair as well as inflammation. Examples of these include: killer cell lectin-like receptors family granzymes and T-cell receptors, which play important roles in host defense. These results support the idea that sleep loss can lead to alteration of molecular processes that drive perturbation of cellular immunity, induction of inflammatory response and homeostatic imbalance. Moreover, down-regulation of multiple genes after prolonged wakefulness (in comparison with baseline condition) and up-regulated after sleep recovery (in comparison with prolonged wakefulness condition) were observed, suggesting an attempt of the body to re-establish internal homeostasis. In silico validation of alterations in the expression of CETN3, DNAJC, IGFR2B and CEACAM genes, confirmed the previous findings related to the molecular effects of sleep deprivation. It is clear that confirmatory studies will be necessary to fully validate the potential candidate genes and functional networks identified. Nevertheless, the present findings confirm that the effects of sleep deprivation are not restricted to the brain and can occur intensely in peripheral tissues. The peripheral blood from each volunteer (nine individuals) were collected in the baseline night and every morning after PW and after the night of SR.

ORGANISM(S): Homo sapiens

SUBMITTER: Renata Pellegrino

PROVIDER: E-GEOD-37667 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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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

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The peripheral genome-wide gene expression profiles in humans after prolonged wakefulness and sleep recovery

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