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Am J Physiol Lung Cell Mol Physiol 280: L107-L115, 2001;
1040-0605/01 $5.00
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Vol. 280, Issue 1, L107-L115, January 2001

Mechanism of dexamethasone-mediated interleukin-8 gene suppression in cultured airway epithelial cells

Mary Mann-Jong Chang1,2,3, Maya Juarez, Dallas M. Hyde1,3, and Reen Wu1,2,3

1 Center for Comparative Respiratory Biology and Medicine, 2 Department of Internal Medicine, School of Medicine, and 3 Department of Anatomy, Physiology, and Cell Biology, School of Veterinary Medicine, University of California, Davis, California 95616

The effects of dexamethasone, a glucocorticoid analog, on interleukin 8 (IL-8) gene expression were studied in cultures of primary human tracheobronchial epithelial cells and an immortalized human bronchial epithelial cell line, HBE1 cells. Dexamethasone inhibited IL-8 mRNA and protein expression in a concentration- and time-dependent manner. The inhibition did not occur at the transcriptional level since both nuclear run-on activity and IL-8 promoter-reporter gene expression assay revealed no significant effect. Instead, there was a change in IL-8 mRNA stability in dexamethasone-treated cultures. Under actinomycin D treatment, IL-8 mRNA was quite stable in dexamethasone-depleted cultures, while in dexamethasone-pretreated cultures, IL-8 message was rapidly degraded within the first hour, then leveled off. When dexamethasone and actinomycin D were added simultaneously to dexamethasone-depleted cultures, IL-8 mRNA remained rather stable. When cycloheximide was used to inhibit new protein synthesis, dexamethasone-dependent inhibition was not observed. These results suggest that a posttranscriptional mechanism, which requires dexamethasone-dependent new protein synthesis, is involved in the regulation of IL-8 mRNA by dexamethasone in airway epithelial cells.

mRNA stability; transcription; posttranscriptional regulation


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