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Most re-endothelialization requires both cell migration and cell proliferation. To study the association between cell migration and the initiation of DNA synthesis in an in vitro wound model, confluent cultures of porcine aortic endothelial cells grown on glass coverslips were scraped to remove half of the monolayer. Treatment with 1 ng/ml of taxol, a microtubule stabilizing drug, for 24 hours resulted in no visible change in F-actin or microtubule organization as assessed by fluorescence and immunofluorescence microscopy. There was, however, a reduction of wound re-endothelialization and an associated reduction in the proportion of cells with centrosomes redistributed toward the wound edge. No significant differences, however, were seen in the labeling indices for the first two rows of cells at the wound edge as revealed by 3H-thymidine autoradiography. Labeling of nuclei in Rows 3 to 8 and in a zone deeper within the monolayer was reduced in treated cultures. The data suggest that endothelial proliferation in cells within an area bordering a wound is dependent on both denudation, which is sufficient to promote maximal proliferation in the two rows adjacent to the wound, and cell migration, which is required for the propagation of proliferation in cells further away from the wound edge.

In vitro endothelial wound repair. Interaction of cell migration and proliferation.