following acute lung injury (ALI) depends on successful
reepithelialization of the denuded alveolar basement membrane, a
process that includes type II alveolar epithelial cell (AEC) migration
on the provisional matrix proteins fibronectin and fibrinogen. We
sought a therapeutic intervention that could accelerate type II AEC
migration after ALI and thus promote alveolar healing. Since hepatocyte
growth factor (HGF) is a potent mitogen for alveolar epithelial cells
and a known motogen for other epithelial cells, we hypothesized that
HGF stimulates AEC migration. The Boyden chemotaxis chamber was
utilized to evaluate the migration of MP48 cells, a type II AEC line.
Filters were coated on the bottom side with either fibronectin or
fibrinogen. Immunofluorescence was performed to demonstrate whether
these cells express HGF or keratinocyte growth factor (KGF) receptors.
MP48 cells migrated on fibronectin, but migrated less on fibrinogen.
HGF stimulated MP48 cell migration on both fibronectin and fibrinogen
in a dose-dependent manner. HGF maximally stimulated migration on
fibronectin by a factor of 9 (p = 0.954 by analysis of variance:
trend for statistical significance) and migration on fibrinogen by a
factor of 8 (p = 0.0233). Of note, KGF, a mitogen for AECs, did not
stimulate migration. Immunofluorescence demonstrated the presence of
both HGF and KGF receptors on these cells. Our results indicate that
HGF augments type II AEC migration on provisional matrix proteins and
thus may be beneficial in promoting alveolar repair following