Freshly isolated rabbit keratinocytes expressed low fibronectin (pFN) receptor function as shown by their poor ability to attach and spread on pFN-coated substrata or to bind and ingest pFN-coated beads. Following in vitro culture of these cells, however, pFN receptor function was activated. The cultured cells appeared to be normal, based on their ability to reepithelialize rapidly full-thickness cutaneous wound beds. Freshly isolated keratinocytes that had low pFN receptor function were autotransplanted onto full-thickness wound beds. Two days after transplantation, keratinocytes recovered from these wounds were observed to express increased pFN receptor function. This activity was maximal in keratinocytes isolated 3 days after transplantation and declined in keratinocytes isolated at later times. By 10 days after transplantation, the transplanted cells had formed a multilayered hyperplastic epidermis and reconstituted their laminin and type IV collagen-containing basement membrane. It is proposed that initiation of pFN receptor function in keratinocytes is a crucial mechanism necessary for them to attach to and migrate through the pFN-rich wound bed comprised of granulation tissue. After reepithelialization is complete, and the basement membrane re-forms, pFN receptor function declines markedly because it is no longer essential to the cells.
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