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Journal of Lipid Research, Vol 37, 2232-2243, Copyright © 1996 by Lipid Research, Inc.

ARTICLES

Glucocorticoid increases rat apolipoprotein A-I promoter activity

AH Taylor, J Raymond, JM Dionne, J Romney, J Chan, DE Lawless, IE Wanke and NC Wong
Department of Medicine, University of Calgary, Alberta, Canada.

The observation that glucocorticoids increase the abundance of apolipoprotein A-I led us to a search for potential underlying mechanism(s). In this report, we show that the synthetic glucocorticoid, dexamethasone, injected into rats increases serum levels of apoA-I protein, hepatic mRNA and "run-on' transcription of the gene by 3-, 5-, and 2-fold, respectively. Results of transient transfection studies of the rat apoA-I promoter reveal that effects of dexamethasone are mediated by a cis-acting site B (-170 to -145). Dexamethasone treatment of hepatoma cells enhances the DNA binding activity of nuclear factors that bind this site. Unexpectedly, site B does not contain a consensus glucocorticoid receptor recognition motif nor binds to bacterially expressed glucocorticoid receptor. These results indicate that the actions of glucocorticoids on site B involve indirect mechanisms. Site B is comprised of a direct repeat of a nonanucleotide and mutation of either one abolishes the effect of glucocorticoid. Additionally, the transcriptional activity of site B in response to dexamethasone is amplified by a 5' sequence called site S (- 186 to -171). Dexamethasone has no effect on site S in the absence of site B. In summary, our data show that dexamethasone increases rat apoA- I gene expression by an indirect mechanism.
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