Glucocorticoid stimulates hepatitis B viral gene expression in cultured human hepatoma cells

Authors

  • Chen-Kung Chou,

    Corresponding author
    1. Department of Medical Research, Veterans General Hospital–Taipei, Taiwan, Republic of China
    2. Graduate Institute of Microbiology, Genetics and Biochemistry, National Yang-Ming Medical College, Taiwan, Republic of China
    3. Institute of Biological Chemistry, Academia Sinica Taipei, Taiwan, Republic of China
    • Department of Medical Research, Veterans General Hospital, Taipei, Taiwan, Republic of China
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  • Li-Hsien Wang,

    1. Graduate Institute of Microbiology, Genetics and Biochemistry, National Yang-Ming Medical College, Taiwan, Republic of China
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  • Hsing-Mei Lin,

    1. Department of Medical Research, Veterans General Hospital–Taipei, Taiwan, Republic of China
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  • Chin-Wen Chi

    1. Department of Medical Research, Veterans General Hospital–Taipei, Taiwan, Republic of China
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Abstract

Glucocorticoids have been shown to influence the severity of hepatitis B virus–related chronic hepatitis in human. However, very little is known about the effects of glucocorticoids on hepatitis B virus replication in vitro. In this report, we used a welldifferentiated human hepatoma cell line, Hep3B, transfected with hepatitis B virus complementary DNA as a model to show that a glucocorticoid analog, dexamethasone, can directly stimulate the production of HBsAg and HBeAg. Elevation of 3.5-kb pregenomic RNA and all other viral RNAs in the transfected Hep3B cells after dexamethasone treatment supports the hypothesis that glucocorticoids directly stimulate hepatitis B virus gene expression in vitro. The concentration of dexamethasone for its half-maximal stimulatory activity toward HBsAg, HBeAg and all viral transcripts was approximately 10–8 mol/L, close to the affinity of glucocorticoid receptors to [3H]triamcinolone acetonide in Hep3B cells ( ± 10–8 mol/L). Specific glucocorticoid antagonist RU38486 completely blocked dexamethasone-induced HBV gene expression, suggesting that the stimulatory effect of dexamethasone was mediated through specific glucocorticoid receptors. (HEPATOLOGY 1992;16:13–18.)

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