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Article: Transforming growth factor-β1 inhibits β2-adrenoceptor gene transcription

TitleTransforming growth factor-β1 inhibits β2-adrenoceptor gene transcription
Authors
Issue Date2000
PublisherSpringer Verlag. The Journal's web site is located at http://link.springer.de/link/service/journals/00210/index.htm
Citation
Naunyn-Schmiedeberg's Archives Of Pharmacology, 2000, v. 362 n. 6, p. 520-525 How to Cite?
AbstractTransforming growth factor-β1 (TGF-β1) has been shown to modulate β-adrenoceptor number and function in cultured human tracheal smooth muscle cells and cardiac fibroblasts, but the mechanism is unclear. In this study, we have characterized the β2-adrenoceptor expression by radioligand binding assay, Northern blot analysis and measurement of intracellular cAMP accumulation in a human embryonic lung fibroblast cell line (HEL299 cells). Treatment with TGF-β1 caused a time-dependent decrease in β2-adrenoceptor mRNA, and in receptor number after 24 h. Furthermore, nuclear run-on assays showed a 35% reduction in the transcription rate of the β2-adrenoceptor gene with no alteration in stability of the β2-adrenoceptor mRNA. After TGF-β1 treatment, the basal, procaterol- and forskolin-stimulated cAMP accumulations were also decreased. Cycloheximide inhibited TGF-β1-mediated reduction of β2-adrenoceptor mRNA and protein, whilst alone caused induction of β2-adrenoceptor mRNA without any effect on receptor number. In summary, TGF-β1 induces β2-adrenoceptor desensitization through the alteration in adenylyl cyclase activity and down-regulation of β2-adrenoceptor mRNA and protein through the reduction in the rate of β2-adrenoceptor gene transcription.
Persistent Identifierhttp://hdl.handle.net/10722/162367
ISSN
2015 Impact Factor: 2.376
2015 SCImago Journal Rankings: 0.859
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorMak, JCWen_US
dc.contributor.authorRousell, Jen_US
dc.contributor.authorHaddad, EBen_US
dc.contributor.authorBarnes, PJen_US
dc.date.accessioned2012-09-05T05:19:19Z-
dc.date.available2012-09-05T05:19:19Z-
dc.date.issued2000en_US
dc.identifier.citationNaunyn-Schmiedeberg's Archives Of Pharmacology, 2000, v. 362 n. 6, p. 520-525en_US
dc.identifier.issn0028-1298en_US
dc.identifier.urihttp://hdl.handle.net/10722/162367-
dc.description.abstractTransforming growth factor-β1 (TGF-β1) has been shown to modulate β-adrenoceptor number and function in cultured human tracheal smooth muscle cells and cardiac fibroblasts, but the mechanism is unclear. In this study, we have characterized the β2-adrenoceptor expression by radioligand binding assay, Northern blot analysis and measurement of intracellular cAMP accumulation in a human embryonic lung fibroblast cell line (HEL299 cells). Treatment with TGF-β1 caused a time-dependent decrease in β2-adrenoceptor mRNA, and in receptor number after 24 h. Furthermore, nuclear run-on assays showed a 35% reduction in the transcription rate of the β2-adrenoceptor gene with no alteration in stability of the β2-adrenoceptor mRNA. After TGF-β1 treatment, the basal, procaterol- and forskolin-stimulated cAMP accumulations were also decreased. Cycloheximide inhibited TGF-β1-mediated reduction of β2-adrenoceptor mRNA and protein, whilst alone caused induction of β2-adrenoceptor mRNA without any effect on receptor number. In summary, TGF-β1 induces β2-adrenoceptor desensitization through the alteration in adenylyl cyclase activity and down-regulation of β2-adrenoceptor mRNA and protein through the reduction in the rate of β2-adrenoceptor gene transcription.en_US
dc.languageengen_US
dc.publisherSpringer Verlag. The Journal's web site is located at http://link.springer.de/link/service/journals/00210/index.htmen_US
dc.relation.ispartofNaunyn-Schmiedeberg's Archives of Pharmacologyen_US
dc.subject.meshAdrenergic Beta-Antagonists - Metabolism - Pharmacologyen_US
dc.subject.meshBinding Sitesen_US
dc.subject.meshBinding, Competitiveen_US
dc.subject.meshBlotting, Northernen_US
dc.subject.meshCell Lineen_US
dc.subject.meshCyclic Amp - Metabolismen_US
dc.subject.meshDown-Regulation - Drug Effectsen_US
dc.subject.meshEmbryo, Mammalianen_US
dc.subject.meshFibroblasts - Drug Effects - Metabolismen_US
dc.subject.meshGene Expressionen_US
dc.subject.meshHumansen_US
dc.subject.meshImidazoles - Metabolism - Pharmacologyen_US
dc.subject.meshIodine Radioisotopesen_US
dc.subject.meshKineticsen_US
dc.subject.meshLung - Drug Effects - Metabolismen_US
dc.subject.meshPindolol - Analogs & Derivatives - Metabolism - Pharmacologyen_US
dc.subject.meshPropanolamines - Metabolism - Pharmacologyen_US
dc.subject.meshRna, Messenger - Genetics - Metabolismen_US
dc.subject.meshRadioligand Assayen_US
dc.subject.meshReceptors, Adrenergic, Beta-2 - Biosynthesis - Genetics - Metabolismen_US
dc.subject.meshTranscription, Genetic - Drug Effectsen_US
dc.subject.meshTransforming Growth Factor Beta - Pharmacologyen_US
dc.subject.meshTransforming Growth Factor Beta1en_US
dc.titleTransforming growth factor-β1 inhibits β2-adrenoceptor gene transcriptionen_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.doi10.1007/s002100000321en_US
dc.identifier.pmid11138844-
dc.identifier.scopuseid_2-s2.0-0033653118en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0033653118&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume362en_US
dc.identifier.issue6en_US
dc.identifier.spage520en_US
dc.identifier.epage525en_US
dc.identifier.isiWOS:000165692300007-
dc.publisher.placeGermanyen_US
dc.identifier.scopusauthoridMak, JCW=7103323094en_US
dc.identifier.scopusauthoridRousell, J=6602560061en_US
dc.identifier.scopusauthoridHaddad, EB=7102803008en_US
dc.identifier.scopusauthoridBarnes, PJ=36064679400en_US

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