We previously gained evidence that Ang-1 and -2 exhibit adverse functions on the recruitment of
inflammatory cells. In particular, Ang-2 promotes the infiltration of myeloid cells upon enduring
expression in settings of inflammation and experimental tumors. Ang-1, in contrast, is able to
antagonize these effects. Brain endothelial cells constitute an important barrier that prevents influx of
cells and substances into the brain. We hypothesize that antagonizing functions of Ang-1 and -2 play an
important role in regulating the blood-brain barrier (BBB). We therefore plan to investigate the effects of
continuous Ang-2 signaling on the BBB functions in health and disease.