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

Citation
Xt. Li et al., Glycosylation profiles of airway epithelium after repair of mechanical injury in guinea pigs, HISTOCHEM J, 32(4), 2000, pp. 207-216
Citations number
28
Categorie Soggetti
Medical Research Diagnosis & Treatment
Journal title
HISTOCHEMICAL JOURNAL
ISSN journal
00182214 → ACNP
Volume
32
Issue
4
Year of publication
2000
Pages
207 - 216
Database
ISI
SICI code
0018-2214(200004)32:4<207:GPOAEA>2.0.ZU;2-K
Abstract
Glycosylated structures on the cell surface have a role in cell adhesion, m igration, and proliferation. Repair of the airway epithelium after injury r equires each of these processes, but the expression of cell surface glycosy lation of airway epithelial cells after injury is not known. We examined ce ll surface glycosylation using lectin-binding profiles of normal and repair ing epithelia in Hartley guinea pigs from 0 to 14 days after mechanical inj ury. The epithelium regenerated completely over 7 days. In normal trachea, galactose- or galactosamine-specific lectins (14 of 20 tested) labelled epi thelial cells, but fucose, mannose, and other sugar-specific lectins (15 te sted) did not. GSA-2, a glucosamine-specific lectin, labelled epithelial ce lls 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 substa ntially after treatment for 24 h with either transforming growth factor-bet a or interleukin-1 beta, but that of the CPA lectin did not. We demonstrate changes in glycosylation profiles of airway epithelial cells coordinate wi th repair after mechanical injury. These changes may be useful to study mec hanisms by which repair is regulated.