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1 Faculty of Medicine, St. Paul's Hospital, University of British Columbia, The James Hogg iCAPTURE Centre for Cardiovascular and Pulmonary Research, Vancouver, Canada
2 Department of Medicine, Division of Biological Sciences, University of Chicago, Section of Pulmonary and Critical Care Medicine, Chicago, Illinois, United States
3 Vancouver, Canada; Faculty of Medicine, St. Paul's Hospital, University of British Columbia, The James Hogg iCAPTURE Centre for Cardiovascular and Pulmonary Research, Vancouver, Canada
* To whom correspondence should be addressed. E-mail: ddorscheid{at}mrl.ubc.ca.
Background: Epithelial repair is a complex cellular and molecular process, the details of which are still not clearly understood. Plasma membrane glycoconjugates can modulate cell function by altering the function of protein and lipids. Sialyl-Lewis x (sLex), a fucose containing tetrasaccharide, decorates membrane bound and secreted proteins and mediates cell-cell interaction. In the present study we investigated the role of sLex in airway epithelial repair.
Methods and Results: Using immunohistochemistry we showed an increased expression of sLex in areas of damaged bronchial epithelium when compared to intact regions. Confluent monolayers of airway epithelial cells were mechanically wounded and allowed to close. Wounded monolayers were photographed for wound closure kinetics, fixed for immunocytochemical studies, or subjected to RNA extraction. Examining the expression of different 
1,3-fucosyltransferases (FucT), enzymes which mediate the final step in the synthesis of sLex, we found that FucT-IV was the common gene expressed in all cell lines and primary airway epithelial cells. We demonstrated an increased expression of sLex over time after mechanical injury. Blocking of sLex with an inhibitory antibody completely prevented epithelial repair.
Conclusion: Our data suggest an essential functional role for sLex in epithelial repair. Further studies are necessary to explore the exact mechanism for sLex in mediating cell-cell interaction in bronchial epithelial cells to facilitate epithelial migration and repair.
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