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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
5
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pubmed:dateCreated |
1997-6-5
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pubmed:abstractText |
Corticotropin-releasing factor (CRF) receptors represent one of the primary sites for negative feedback of the pituitary by adrenocortical glucocorticoid hormones; however, the molecular mechanisms involved have yet to be elucidated. The present study examines the mechanisms by which glucocorticoids regulate CRF-R1 expression in the pituitary cell line, AtT-20. Treatment of these cells with dexamethasone resulted in a concentration- and time-dependent inhibition of CRF-R1 mRNA that was significant by 1 hr and maximal after 4 hr. Levels of CRF-R1 mRNA then returned to control levels after 24 hr. Similar changes were observed when the cells were treated with corticosterone. Pro-opiomelanocortin mRNA was also decreased after dexamethasone pretreatment; however, the time course was much slower with a significant effect only detected after 6 hr. Further analysis of the mechanisms that mediate glucocorticoid regulation of CRF-R1 mRNA was conducted These studies demonstrated that glucocorticoid incubation significantly decreases the rate of CRF-R1 gene transcription, as determined by nuclear run-on analysis. In addition, the result demonstrate that glucocorticoid incubation significantly decreases CRF-R1 mRNA stability by approximately 50%. The down-regulation of CRF-R1 mRNA was dependent on de novo protein synthesis, as it was blocked by pretreatment with cycloheximide. This represents a novel mechanism for glucocorticoid negative feedback regulation of CRF-R1 expression.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
|
pubmed:month |
May
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pubmed:issn |
0026-895X
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pubmed:author | |
pubmed:issnType |
Print
|
pubmed:volume |
51
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pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
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pubmed:pagination |
794-9
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:9145917-Cell Line,
pubmed-meshheading:9145917-Dexamethasone,
pubmed-meshheading:9145917-Gene Expression Regulation,
pubmed-meshheading:9145917-Pituitary Gland,
pubmed-meshheading:9145917-RNA, Messenger,
pubmed-meshheading:9145917-Receptors, Corticotropin-Releasing Hormone,
pubmed-meshheading:9145917-Transcription, Genetic
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pubmed:year |
1997
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pubmed:articleTitle |
Glucocorticoid regulation of corticotropin-releasing factor1 receptor expression in pituitary-derived AtT-20 cells.
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pubmed:affiliation |
Department of Psychiatry, Yale University School of Medicine, Connecticut Mental Health Center, New Haven 06508, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, U.S. Gov't, Non-P.H.S.
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