Sleep Deprivation Compromises Lacrimal System and Homeostasis of the Ocular Surface

Abstract

Purpose : Normal sleep plays a pivotal role in mental and physiological health of human being. Sleep deficiency and deprivation are associated with various systemic diseases such as obesity and cardiovascular disease. This study was conducted to investigate the effect of sleep deprivation on ocular surface tissues in a mouse model.

Methods :
Adult C57BL/6 mice were used to establish a sleep deprivation mouse model using modified “stick over water” method. Slit-lamp microscope observation, fluorescein test, and Schirmer’s tear secretion test were performed to detect ocular surface and tear film change of the animals. Hematoxylin-Eosin, Oil Red O staining, cell apoptosis detection, immunofluorescence staining, Periodic Acid-Schiff (PAS) staining were performed on lacrimal gland and ocular surface tissues. LC/MS/MS analysis was performed to detect amino acids in lacrimal gland tissues. Quantitative real-time RT-PCR analysis was performed to detect gene expression in cornea and lacrimal gland.

Results : Mice exhibited aqueous tear secretion decrease, corneal epithelial defect and apoptosis, corneal squamous metaplasia, as well as hypertrophic changes of lacrimal gland acinar cells after sleep deprivation for different durations. Further investigation showed increased inflammatory cytokine expression, abnormal lipid metabolism and decreased protein synthesis of lacrimal gland after sleep deprivation.

Conclusions :
The pathological changes of mice after sleep deprivation mimic dry eye manifestations. These mice may be valuable model to study the pathophysiological process and mechanism of sleep disorder related ocular surface diseases.

This is an abstract that was submitted for the 2017 ARVO Annual Meeting, held in Baltimore, MD, May 7-11, 2017.