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

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. A total of 12 samples from cerebral cortex endothelial cells of male C57BL/6J mice were analyzed. Sleep deprivation was induced using a rotarod at 6 rpm for 6, 12, or 24 hours, with interventions starting at 08:00 am. Endothelial cells were isolated by magnetic-activated cell sorting (MACS) with CD31 microbeads. The control group underwent no interventions and was maintained under normal housing conditions.