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Am. J. Respir. Cell Mol. Biol., Volume 19, Number 3, September, 1998 357-365

Ozone Alters the Distribution of beta 1 Integrins in Cultured Primate Bronchial Epithelial Cells

Abdallah J. Jabbour, Leonard C. Altman, Thomas N. Wight, and Daniel L. Luchtel

Department of Environmental Health; Division of Allergy and Infectious Diseases; and Department of Pathology, Department of Medicine, University of Washington, Seattle, Washington

The effects of 0.5 ppm ozone exposure for 6 h on the synthesis and distribution of beta 1 integrins were examined in bronchial epithelial cells cultured at an air-cell interface. Ozone exposure damaged cilia and caused significant cell loss. Immunocytochemical localization and quantification of the beta 1 subunit in the remaining attached cells using scanning laser cytometry demonstrated time-dependent changes in beta 1 distribution in response to ozone. Although no changes were detected immediately after exposure, beta 1 immunoreactivity increased 23 ± 5% and 66 ± 6% at 6 and 24 h, respectively. The increased immunostaining was localized at the apical surfaces and, to a lesser extent, at cell-cell contacts of cultured cells. Furthermore, integrin redistribution was not due to increased messenger RNA (mRNA) levels and protein synthesis because levels of beta 1 mRNA and newly synthesized beta 1 protein did not change after ozone exposure. However, immunoprecipitation analysis of beta 1 integrins in lysates from equal numbers of cells showed that ozone-exposed cells contained 90 ± 15% more total beta 1 subunit at 24 h after exposure. In addition, our results demonstrated the presence of the alpha 5beta 1 integrin complex in bronchial epithelial cells and that the detergent-soluble amount of its associated beta 1 subunit increased 60 ± 10% in lysates of ozone-exposed cells. In conclusion, ozone altered cellular distribution of beta 1 integrins in the remaining attached cells subsequent to cell injury and loss. The changes in beta 1 distribution might be due to increased detergent extractibility of beta 1 integrins rather than a real increase in the synthesis of beta 1 integrins.




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Copyright © 1998 American Thoracic Society.