File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Glucocorticosteroids increase β2-adrenergic receptor transcription in human lung

TitleGlucocorticosteroids increase β2-adrenergic receptor transcription in human lung
Authors
Issue Date1995
PublisherAmerican Physiological Society. The Journal's web site is located at http://intl-ajplung.physiology.org/
Citation
American Journal Of Physiology - Lung Cellular And Molecular Physiology, 1995, v. 268 n. 1 12-1, p. L41-L46 How to Cite?
Abstractβ2-Adrenergic receptors (β2R) are widely distributed and mediate a wide range of cellular responses in lung. Because glucocorticosteroids increase expression of β2R in cell lines, we have investigated the effects of glucocorticoids on the β2R mRNA level and the number of β2R in human peripheral lung in vitro. Incubation of lung tissues with dexamethasone (Dex) elevated both β2R mRNA level (as measured by Northern blot analysis) and β2R number (as measured by [125I]iodocyanopindolol binding). The increased accumulation of β2R mRNA could be detected at 15 min (1.27 ± 0.1-fold) and the maximal accumulation occurred at 2 h (2.73 ± 0.5-fold). The Dex-induced increase in β2R mRNA returned to the control level by 17 h. The increase in β2R number (1.58 ± 0.2-fold) was slower, reaching a maximum between 17 and 24 h. Dex increased β2R mRNA in a time- and concentration-dependent manner that was abolished by the steroid receptor antagonist mifepristone (RU-38486 or RU-486). The stability of β2R mRNA was unchanged by Dex, and a nuclear run-on assay revealed that Dex approximately doubled the transcriptional rate of the β2R gene. These observations suggest that glucocorticoids act on steroid receptors to increase β2R expression by increasing the rate of β2R gene transcription.
Persistent Identifierhttp://hdl.handle.net/10722/162065
ISSN
2015 Impact Factor: 4.721
2015 SCImago Journal Rankings: 1.838
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorMak, JCWen_US
dc.contributor.authorNishikawa, Men_US
dc.contributor.authorBarnes, PJen_US
dc.date.accessioned2012-09-05T05:17:01Z-
dc.date.available2012-09-05T05:17:01Z-
dc.date.issued1995en_US
dc.identifier.citationAmerican Journal Of Physiology - Lung Cellular And Molecular Physiology, 1995, v. 268 n. 1 12-1, p. L41-L46en_US
dc.identifier.issn1040-0605en_US
dc.identifier.urihttp://hdl.handle.net/10722/162065-
dc.description.abstractβ2-Adrenergic receptors (β2R) are widely distributed and mediate a wide range of cellular responses in lung. Because glucocorticosteroids increase expression of β2R in cell lines, we have investigated the effects of glucocorticoids on the β2R mRNA level and the number of β2R in human peripheral lung in vitro. Incubation of lung tissues with dexamethasone (Dex) elevated both β2R mRNA level (as measured by Northern blot analysis) and β2R number (as measured by [125I]iodocyanopindolol binding). The increased accumulation of β2R mRNA could be detected at 15 min (1.27 ± 0.1-fold) and the maximal accumulation occurred at 2 h (2.73 ± 0.5-fold). The Dex-induced increase in β2R mRNA returned to the control level by 17 h. The increase in β2R number (1.58 ± 0.2-fold) was slower, reaching a maximum between 17 and 24 h. Dex increased β2R mRNA in a time- and concentration-dependent manner that was abolished by the steroid receptor antagonist mifepristone (RU-38486 or RU-486). The stability of β2R mRNA was unchanged by Dex, and a nuclear run-on assay revealed that Dex approximately doubled the transcriptional rate of the β2R gene. These observations suggest that glucocorticoids act on steroid receptors to increase β2R expression by increasing the rate of β2R gene transcription.en_US
dc.languageengen_US
dc.publisherAmerican Physiological Society. The Journal's web site is located at http://intl-ajplung.physiology.org/en_US
dc.relation.ispartofAmerican Journal of Physiology - Lung Cellular and Molecular Physiologyen_US
dc.subject.meshAdolescenten_US
dc.subject.meshAdulten_US
dc.subject.meshDexamethasone - Pharmacologyen_US
dc.subject.meshDrug Stabilityen_US
dc.subject.meshFemaleen_US
dc.subject.meshHumansen_US
dc.subject.meshLung - Cytology - Drug Effects - Physiologyen_US
dc.subject.meshMaleen_US
dc.subject.meshOsmolar Concentrationen_US
dc.subject.meshRna, Messenger - Metabolismen_US
dc.subject.meshReceptors, Adrenergic, Beta - Drug Effects - Genetics - Metabolismen_US
dc.subject.meshTranscription, Genetic - Drug Effectsen_US
dc.titleGlucocorticosteroids increase β2-adrenergic receptor transcription in human lungen_US
dc.typeArticleen_US
dc.identifier.emailMak, JCW:judymak@hku.hken_US
dc.identifier.authorityMak, JCW=rp00352en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.pmid7840227-
dc.identifier.scopuseid_2-s2.0-0028821223en_US
dc.identifier.volume268en_US
dc.identifier.issue1 12-1en_US
dc.identifier.spageL41en_US
dc.identifier.epageL46en_US
dc.identifier.isiWOS:A1995QB29200008-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridMak, JCW=7103323094en_US
dc.identifier.scopusauthoridNishikawa, M=7402607361en_US
dc.identifier.scopusauthoridBarnes, PJ=36064679400en_US

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats