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1 McDonald Research Laboratory, University of British Columbia, Vancouver, British Columbia V6Z 1Y6, Canada; and 2 Section of Pulmonary and Critical Care Medicine, Department of Medicine, Division of Biological Sciences, University of Chicago, Chicago, Illinois 60637
Our laboratory recently demonstrated
the pattern of cell surface glycosylation of nonsecretory central
airway epithelium (Dorscheid DR, Conforti AE, Hamann KJ, Rabe KF, and
White SR. Histochem J 31: 145-151, 1999), but the role
of glycosylation in airway epithelial cell migration and repair is
unknown. We examined the functional role of cell surface carbohydrates
in wound repair after mechanical injury of 1HAEo
human
airway epithelial and primary bronchial epithelial monolayers. Wound
repair stimulated by epidermal growth factor was substantially attenuated by 10
7 M tunicamycin (TM), an N-glycosylation
inhibitor, but not by the inhibitors deoxymannojirimycin or
castanospermine. Wound repair of 1HAEo
and primary airway
epithelial cells was blocked completely by removal of cell surface
terminal fucose residues by
-fucosidase. Cell adhesion to collagen
matrix was prevented by TM but was only reduced ~20% from control
values with prior
-fucosidase treatment. Cell migration in Blind
Well chambers stimulated by epidermal growth factor was blocked by
pretreatment with TM but
-fucosidase pretreatment produced no
difference from control values. These data suggest that cell surface
N-glycosylation has a functional role in airway epithelial cell
adhesion and migration and that N-glycosylation with terminal
fucosylation plays a role in the complex process of repair by
coordination of certain cell-cell functions.
epithelium; tunicamycin; fucosidase; cell migration; cell adhesion; cell spreading
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