Abstract
Attachment and migration of fibroblasts to the vitronectin- and fibronectin-rich alveolar matrices are critical processes in wound repair after acute lung injury. This study was undertaken to determine the mechanism by which human lung fibroblasts attach and migrate toward provisional alveolar matrix proteins, and to develop mechanism-based, novel therapeutic agents designed to specifically inhibit these functions. We have previously demonstrated urokinase plasminogenactivator receptor (u-PAR) and a functional fibrinolytic system on these cells.
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