The mechanism and regulation of reendothelialization of small aortic endothelial
wounds is not well understood. An in vitro model system was designed to study the repair of a
wound created by the removal of a single endothelial cell from a confluent monolayer. Time-lapse cinemicrophotography was used to characterize the kinetics of
wound repair. Because all of the endothelial cells adjacent to the
wound extruded lamellipodia to rapidly close the
wound within 30 to 45 minutes, the repair process was referred to descriptively as rapid lamellipodia-mediated
wound closure. Treatment of the wounded cultures with
cytochalasin B resulted in a marked decrease in lamellipodia extrusion and a significant delay in
wound closure. Washout of
cytochalasin B resulted in the reappearance of lamellipodia extrusion and the rapid closure of the
wound. Localization of actin microfilaments by
7-nitrobenz-2-oxa-1,3-diazole phallicidin in control and
cytochalasin B-treated
wounds showed that rapid lamellipodia-mediated
wound closure was associated with the presence of a dense peripheral band of actin microfilament bundles normally located around the periphery of each endothelial cell in the confluent monolayer. The results suggest that the process of single-cell
wound repair is a function of lamellipodial extrusion which itself may be regulated, at least in part, by the actin-containing dense peripheral band of microfilament bundles located at the periphery of endothelial cells in confluent monolayers.