INVITRO REENDOTHELIALIZATION OF A SINGLE-CELL WOUND - ROLE OF MICROFILAMENT BUNDLES IN RAPID LAMELLIPODIA-MEDIATED WOUND CLOSURE

  • 1 January 1984
    • journal article
    • research article
    • Vol. 51  (1) , 75-81
Abstract
The mechanism and regulation of reendothelialization of small aortic endothelial wounds is not well understood. An in vitro model system [in pigs] 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 30-45 min, 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 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.