Glycosylation profiles of airway epithelium after repair of mechanical injury in guinea pigs

• Published in: Journal of molecular histology Vol. 32; no. 4; pp. 207 - 216
• Main Authors: Xiantang, L, Dorscheid, D R, Wojcik, K R, White, S R
• Format: Journal Article
• Language: English
• Published: Netherlands Springer Nature B.V 01.04.2000
• Subjects: Animals; Blotting, Western - methods; Cells; Glycosylation; Guinea Pigs; Lectins - metabolism; Male; Proteins; Respiratory Mucosa - injuries; Respiratory Mucosa - metabolism; Respiratory Mucosa - pathology; Trachea - injuries; Trachea - metabolism; Trachea - pathology
• ISSN: 0018-2214; 1567-2379; 1567-2387
• DOI: 10.1023/A:1004046816516

Glycosylated structures on the cell surface have a role in cell adhesion, migration, and proliferation. Repair of the airway epithelium after injury requires each of these processes, but the expression of cell surface glycosylation of airway epithelial cells after injury is not known. We examined cell surface glycosylation using lectin-binding profiles of normal and repairing epithelia in Hartley guinea pigs from 0 to 14 days after mechanical injury. The epithelium regenerated completely-over 7 days. In normal trachea, galactose- or galactosamine-specific lectins (14 of 20 tested) labelled epithelial cells, but fucose, mannose, and other sugar-specific lectins (15 tested) did not. GSA-2, a glucosamine-specific lectin, labelled epithelial cells weakly in uninjured tracheas, but intense labelling was noted in basal and non-ciliated columnar cells adjacent to the injury site over 3 h to 14 days after injury. Labelling of these cells peaked at 12 h and 5 days after injury respectively. Similar patterns were seen with lectins AlloA and HAA but not with CPA during repair. The binding of the lectin DSA to proteins collected from primary cultures of airway epithelial cells decreased substantially after treatment for 24 h with either transforming growth factor-beta or interleukin-1beta, but that of the CPA lectin did not. We demonstrate changes in glycosylation profiles of airway epithelial cells coordinate with repair after mechanical injury. These changes may be useful to study mechanisms by which repair is regulated.