Abstract
Repair of the airway epithelium after injury involves cell proliferation, migration, and spreading into the injury site. The growth factor, epidermal growth factor (EGF), elicits proliferation of many epithelial cell types in vitro and in vivo, including airways epithelium. However, its effects on cell migration and spreading are less clear. We studied the effects of EGF on guinea-pig tracheal epithelial cell (GPTEC) chemotaxis and migration during wound repair. Primary GPTEC were allowed to migrate through a gelatin-coated filter for 6 h in a chemotaxis chamber, after which the number of migrated cells were counted. EGF elicited migration of GPTEC that was substantial and concentration-dependent. Treatment with EGF accelerated closure of small wounds in confluent epithelial monolayers substantially as measured by video microscopy over 24 h. These effects of EGF were concentration-dependent and seen in monolayer wounds of different size. Effects of EGF did not depend on the underlying matrix on which cells were grown; cells grown on laminin, fibronectin, or collagen had similar wound closure velocities in response to EGF. Early effects of EGF on wound closure were not due to cell proliferation at the wound edge. These data demonstrate that EGF elicits both chemotaxis and migration of airway epithelial cells in culture.
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