Intermittent
hypoxia is a major factor in clinical conditions like the
obstructive sleep apnea syndrome or the cyclic recruitment and derecruitment of
atelectasis in
acute respiratory distress syndrome and positive pressure
mechanical ventilation. In vivo investigations of the direct impact of intermittent
hypoxia are frequently hampered by multiple co-morbidities of patients. Therefore, cell culture experiments are important model systems to elucidate molecular mechanisms that are involved in the cellular response to alternating
oxygen conditions and could represent future targets for tailored
therapies. In this study, we focused on mouse lung endothelial cells as a first frontier to encounter altered
oxygen due to disturbances in airway or lung function, that play an important role in the development of secondary diseases like
vascular disease and
pulmonary hypertension. We analyzed key markers for endothelial function including
cell adhesion molecules, molecules involved in regulation of fibrinolysis, hemostasis, redox balance, and regulators of gene expression like
miRNAs. Results show that short-time exposure to intermittent
hypoxia has little impact on vitality and health of cells. At early timepoints and up to 24 h, many endothelial markers are unchanged in their expression and some indicators of injury are even downregulated. However, in the long-term, multiple signaling pathways are activated, that ultimately result in cellular
inflammation, oxidative stress, and apoptosis.