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rdf:type |
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lifeskim:mentions |
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pubmed:dateCreated |
1994-10-14
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pubmed:abstractText |
The expression of beta 2-adrenergic receptors is up-regulated by glucocorticoids. In contrast, beta 1-adrenergic receptors display glucocorticoid-induced down-regulation. In rat C6 glioma cells, which express both of these subtypes of beta-adrenergic receptors, the synthetic glucocorticoid dexamethasone stimulates no change in the total beta-adrenergic receptor content, but rather shifts the beta 1:beta 2 ratio from 80:20 to 50:50. Radioligand binding and immunoblotting demonstrate a sharp decline in beta 1-adrenergic receptor expression. Metabolic labelling of cells with [35S]-methionine in tandem with immunoprecipitation by beta 1-adrenergic-receptor-specific antibodies reveals a sharp decline in the synthesis of the receptor within 48 h for cells challenged with glucocorticoid. Steady-state levels of beta 1-adrenergic-receptor mRNA declined from 0.47 to 0.26 amol/microgram of total cellular RNA within 2 h of dexamethasone challenge, as measured by DNA-excess solution hybridization. The stability of receptor mRNA was not influenced by glucocorticoid; the half-lives of the beta 1- and beta 2-subtype mRNAs were 1.7 and 1.5 h respectively. Nuclear run-on assays revealed the basis for the down-regulation of receptor expression, i.e. a sharp decline in the relative rate of transcription for the beta 1-adrenergic-receptor gene in nuclei from dexamethasone-treated as compared with vehicle-treated cells. These data demonstrate transcriptional suppression as a molecular explanation for glucocorticoid-induced down-regulation of beta 1-adrenergic receptors.
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/8092990-1323234,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8092990-1649740,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8092990-1651924,
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Sep
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pubmed:issn |
0264-6021
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
302 ( Pt 2)
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
397-403
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:8092990-Animals,
pubmed-meshheading:8092990-Base Sequence,
pubmed-meshheading:8092990-Cricetinae,
pubmed-meshheading:8092990-Dexamethasone,
pubmed-meshheading:8092990-Down-Regulation,
pubmed-meshheading:8092990-Electrophoresis, Polyacrylamide Gel,
pubmed-meshheading:8092990-Gene Expression Regulation,
pubmed-meshheading:8092990-Glioma,
pubmed-meshheading:8092990-Immunoblotting,
pubmed-meshheading:8092990-Molecular Sequence Data,
pubmed-meshheading:8092990-Nucleic Acid Hybridization,
pubmed-meshheading:8092990-Precipitin Tests,
pubmed-meshheading:8092990-RNA, Messenger,
pubmed-meshheading:8092990-Radioligand Assay,
pubmed-meshheading:8092990-Rats,
pubmed-meshheading:8092990-Receptors, Adrenergic, beta,
pubmed-meshheading:8092990-Transcription, Genetic,
pubmed-meshheading:8092990-Tumor Cells, Cultured
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pubmed:year |
1994
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pubmed:articleTitle |
Glucocorticoids down-regulate beta 1-adrenergic-receptor expression by suppressing transcription of the receptor gene.
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pubmed:affiliation |
Department of Molecular Pharmacology, School of Medicine, University at Stony Brook, NY 11794-8651.
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pubmed:publicationType |
Journal Article
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