Abstract
The primary cilium is present on the surface of most cells in the body. In the vascular system, it is particularly important in endothelial cells, where it senses shear stress and regulates many aspects of vascular function. In pathologies such as atherosclerosis, a loss or reduction in the number and length of cilia is observed. Here, we demonstrate that the loss of primary cilia, induced by pharmacological treatments, results in part from the release of EVs from these cilia. These EVs have been characterized and we show that they are enriched in primary cilia markers. Interestingly, these EVs were associated with increased production of reactive oxygen species (ROS) in endothelial cells, without altering NO bioavailability. Furthermore, we observed that ciliated cell-derived EVs increased cell migration and prevented the TNFα-induced increase in endothelial cell permeability. Finally, we show that EVs from obstructive sleep apnea syndrome (OSAS) patients with endothelial dysfunction express more primary cilia markers, suggesting that these EVs could serve as biomarkers of endothelial dysfunction. Taken together, these results highlight the role of primary cilia EVs in impaired endothelial function associated with increased oxidative stress, and their potential use as biomarkers of cardiovascular disease.