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Acute Sleep Deprivation Accelerates Brain Endothelial Cell Senescence and Functional Changes of Endothelial Cells in Mice

ABSTRACT: Sleep, a fundamental physiological process occupying approximately one - third of the human lifespan, is essential for maintaining overall health. Acute sleep deprivation (ASD), a prevalent condition in modern society, has been strongly associated with the pathogenesis of various neurodegenerative diseases. Endothelial cells play a pivotal role in regulating vascular tone, modulating inflammatory responses, and maintaining barrier integrity. While previous research has indicated that sleep deprivation can contribute to endothelial cell dysfunction, potentially leading to the development of atherosclerosis, hypertension, and other vascular disorders, the precise effects of ASD on brain endothelial cells and the underlying molecular mechanisms remain incompletely understood. Our study focuses on exploring the specific effects of acute sleep deprivation on the phenotypic characteristics and molecular functions of brain endothelial cells. Through bioinformatics analysis and multiple experimental approaches, it reveals the close relationship between acute sleep deprivation and endothelial cell senescence as well as alterations in molecular functions. By uncovering the molecular change, we provides a theoretical basis and novel perspectives for the research and treatment of related diseases.

ORGANISM(S): Mus musculus

PROVIDER: GSE299158 | GEO | 2025/06/07

REPOSITORIES: GEO

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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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Acute Sleep Deprivation Accelerates Brain Endothelial Cell Senescence and Functional Changes of Endothelial Cells in Mice

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