Intermittent and sustained hypoxia exposures activate distinct transcriptional responses in human aortic endothelial cells

Endothelial cell (EC) dysfunction precedes the development of cardiovascular disease in OSA; however, the mechanisms by which ECs respond to these hypoxic events is poorly understood. To better understand EC responses to hypoxia, we examined the effects of both sustained hypoxia (SH) and intermittent hypoxia (IH) on the activation of HIF-1a in Endothelial Cells (ECs). While SH stabilized HIF-1a and led to its nuclear localization, IH didn't activate HIF-1a and its downsteram gene expression. Using RNA-sequencing, we evaluated transcriptional responses of ECs to hypoxia. SH induced expression of HIF-1a and hypoxia response genes, while IH affected cell-cycle regulation genes. Overall design: HAEC cells