OZONE ALTERS THE DISTRIBUTION OF BETA(1) INTEGRINS IN CULTURED PRIMATE BRONCHIAL EPITHELIAL-CELLS

Citation
Aj. Jabbour et al., OZONE ALTERS THE DISTRIBUTION OF BETA(1) INTEGRINS IN CULTURED PRIMATE BRONCHIAL EPITHELIAL-CELLS, American journal of respiratory cell and molecular biology, 19(3), 1998, pp. 357-365
Citations number
48
Categorie Soggetti
Cell Biology",Biology,"Respiratory System
ISSN journal
10441549
Volume
19
Issue
3
Year of publication
1998
Pages
357 - 365
Database
ISI
SICI code
1044-1549(1998)19:3<357:OATDOB>2.0.ZU;2-Z
Abstract
The effects of 0.5 ppm ozone exposure for 6 h on the synthesis and dis tribution of beta(1) integrins were examined in bronchial epithelial c ells cultured at an air-cell interface. Ozone exposure damaged cilia a nd caused significant cell loss. Immunocytochemical localization and q uantification of the beta(1) subunit in the remaining attached cells u sing scanning laser cytometry demonstrated time-dependent changes in b eta(1) distribution in response to ozone. Although no changes were det ected immediately after exposure, beta(1) immunoreactivity increased 2 3 +/- 5% and 66 +/- 6% at 6 and 24 h, respectively. The increased immu nostaining was localized at the apical surfaces and, to a lesser exten t, at cell-cell contacts of cultured cells. Furthermore, integrin redi stribution was not due to increased messenger RNA (mRNA) levels and pr otein synthesis because levels of beta(1) mRNA and newly synthesized b eta(1) protein did not change after ozone exposure. However, immunopre cipitation analysis of beta(1) integrins in lysates from equal numbers of cells showed that ozone-exposed cells contained 90 +/- 15% more to tal beta(1) subunit at 24 h after exposure. In addition, our results d emonstrated the presence of the alpha(5)beta(1) integrin complex in br onchial epithelial cells and that the detergent-soluble amount of its associated beta(1) subunit increased 60 +/- 10% in lysates of ozone-ex posed cells. In conclusion, ozone altered cellular distribution of bet a(1) integrins in the remaining attached cells subsequent to cell inju ry and loss. The changes in beta(1) distribution might be due to incre ased detergent extractibility of beta(1) integrins rather than a real increase in the synthesis of beta(1) integrins.