Differences in Down-Regulation of Glucocorticoid Receptor mRNA by Cortisol Prednisolone and Dexamethasone in HeLa Cells
Glucocorticoids regulate the levels of their cognate receptors in a number of target tissues and in many different cell lines. We have compared the effect of three glucocorticoids, cortisol and its synthetic derivatives, prednisolone and dexamethasone, on the levels of glucocorticoid receptor (GR) m...
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Published in | ENDOCRINE JOURNAL Vol. 42; no. 5; pp. 629 - 636 |
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Main Authors | , , , , , |
Format | Journal Article |
Language | English Japanese |
Published |
Japan
The Japan Endocrine Society
1995
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Subjects | |
Online Access | Get full text |
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Summary: | Glucocorticoids regulate the levels of their cognate receptors in a number of target tissues and in many different cell lines. We have compared the effect of three glucocorticoids, cortisol and its synthetic derivatives, prednisolone and dexamethasone, on the levels of glucocorticoid receptor (GR) mRNA in HeLa cells. Clinically, the synthetic derivatives are more active in hormonal action and have a longer half-life than cortisol. In the present study, the amounts of GR mRNA in HeLa cells were examined by Northern blot hybridization after treatment with cortisol, prednisolone or dexamethasone. These glucocorticoids decreased GR mRNA levels differently. After 24h treatment with 1×10-5M cortisol, GR mRNA levels were only marginally suppressed (90% of the control), while prednisolone and dexamethasone suppressed GR mRNA levels to 67 and 57%, respectively. These differences may relate to the biological activities of these glucocorticoids. In time course studies, GR mRNA levels of the cells treated with cortisol and prednisolone decreased to the minimum levels within 4h and then recovered gradually, while those treated with dexamethasone reached the minimum level at 8h and remained suppressed for more than 24h. These differences may relate to the biological half-lives of these glucocorticoids. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0918-8959 1348-4540 |
DOI: | 10.1507/endocrj.42.629 |