OASL and endothelial dysfunction: Moreover, monocyte adhesion (Fig. 4e) and transmigration (Fig. 4f) were enhanced in Oasl1−/− MAECs compared with controls, indicating that the loss of endothelial Oasl1 promotes endothelial dysfunction, with the concomitant occurrence of a positive feedback loop of increased inflammation, leukocyte adhesion, and infiltration.