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Article: Up-regulation of airway smooth muscle histamine H1 receptor mRNA, protein, and function by β2-adrenoceptor activation

TitleUp-regulation of airway smooth muscle histamine H1 receptor mRNA, protein, and function by β2-adrenoceptor activation
Authors
Issue Date2000
PublisherAmerican Society for Pharmacology and Experimental Therapeutics. The Journal's web site is located at http://www.molpharm.org
Citation
Molecular Pharmacology, 2000, v. 57 n. 5, p. 857-864 How to Cite?
AbstractHistamine, released from activated mast cells, causes bronchoconstriction mediated by H1 receptors, whereas β2-agonists are widely used for the relief of bronchoconstriction. In this study, we examined the effects of the β2-adrenoceptor agonist, fenoterol, on the expression of H1 receptors at the mRNA and protein levels, and functional responses, incubation of bovine tracheal smooth muscle with fenoterol (10-7 M) for 2 h increased H1 receptor mRNA (maximum ~190%). The number of H1 receptors was increased after 12 and 18 h without any change in binding affinity. In the contraction experiments, the concentration-response curves for histamine- induced contraction were shifted significantly to the left after 18-h exposure to fenoterol, consistent with the increase in receptor number. The fenoterol-induced increase in H1 receptor mRNA was concentration-dependent and was abolished by propranolol and ICI 118551, but not by CGP 20712A, indicating that fenoterol acts via β2-adrenoceptors. These effects were mimicked by other cAMP-elevating agents forskolin and prostaglandin E2, and by the stable cAMP analog 8-bromo-cAMP. Cycloheximide alone produced superinduction of H1 receptor mRNA and augmented the fenoterol-induced increase in H1 receptor mRNA. Fenoterol increased both the stability and the transcription rate of H1 receptor mRNA. Pretreatment with dexamethasone did not prevent fenoterol-induced up-regulation of H1 receptor mRNA. Thus, fenoterol increases the expression of airway smooth muscle H1 receptors via activation of the cAMP system through increased gene transcription and mRNA stability. This mechanism may be involved in the adverse responses encountered with the clinical use of short-acting β2-agonists.
Persistent Identifierhttp://hdl.handle.net/10722/162416
ISSN
2015 Impact Factor: 3.931
2015 SCImago Journal Rankings: 2.047
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorMak, JCWen_US
dc.contributor.authorRoffel, AFen_US
dc.contributor.authorKatsunuma, Ten_US
dc.contributor.authorElzinga, CRSen_US
dc.contributor.authorZaagsma, Jen_US
dc.contributor.authorBarnes, PJen_US
dc.date.accessioned2012-09-05T05:19:44Z-
dc.date.available2012-09-05T05:19:44Z-
dc.date.issued2000en_US
dc.identifier.citationMolecular Pharmacology, 2000, v. 57 n. 5, p. 857-864en_US
dc.identifier.issn0026-895Xen_US
dc.identifier.urihttp://hdl.handle.net/10722/162416-
dc.description.abstractHistamine, released from activated mast cells, causes bronchoconstriction mediated by H1 receptors, whereas β2-agonists are widely used for the relief of bronchoconstriction. In this study, we examined the effects of the β2-adrenoceptor agonist, fenoterol, on the expression of H1 receptors at the mRNA and protein levels, and functional responses, incubation of bovine tracheal smooth muscle with fenoterol (10-7 M) for 2 h increased H1 receptor mRNA (maximum ~190%). The number of H1 receptors was increased after 12 and 18 h without any change in binding affinity. In the contraction experiments, the concentration-response curves for histamine- induced contraction were shifted significantly to the left after 18-h exposure to fenoterol, consistent with the increase in receptor number. The fenoterol-induced increase in H1 receptor mRNA was concentration-dependent and was abolished by propranolol and ICI 118551, but not by CGP 20712A, indicating that fenoterol acts via β2-adrenoceptors. These effects were mimicked by other cAMP-elevating agents forskolin and prostaglandin E2, and by the stable cAMP analog 8-bromo-cAMP. Cycloheximide alone produced superinduction of H1 receptor mRNA and augmented the fenoterol-induced increase in H1 receptor mRNA. Fenoterol increased both the stability and the transcription rate of H1 receptor mRNA. Pretreatment with dexamethasone did not prevent fenoterol-induced up-regulation of H1 receptor mRNA. Thus, fenoterol increases the expression of airway smooth muscle H1 receptors via activation of the cAMP system through increased gene transcription and mRNA stability. This mechanism may be involved in the adverse responses encountered with the clinical use of short-acting β2-agonists.en_US
dc.languageengen_US
dc.publisherAmerican Society for Pharmacology and Experimental Therapeutics. The Journal's web site is located at http://www.molpharm.orgen_US
dc.relation.ispartofMolecular Pharmacologyen_US
dc.subject.meshAdrenergic Beta-Agonists - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBlotting, Northernen_US
dc.subject.meshCattleen_US
dc.subject.meshFenoterol - Pharmacologyen_US
dc.subject.meshGlucocorticoids - Pharmacologyen_US
dc.subject.meshMuscle Contraction - Drug Effectsen_US
dc.subject.meshMuscle, Smooth - Drug Effects - Metabolismen_US
dc.subject.meshRna, Messenger - Metabolismen_US
dc.subject.meshRadioligand Assayen_US
dc.subject.meshReceptors, Adrenergic, Beta-2 - Metabolismen_US
dc.subject.meshReceptors, Histamine H1 - Genetics - Metabolismen_US
dc.subject.meshTrachea - Drug Effects - Metabolismen_US
dc.subject.meshUp-Regulation - Drug Effectsen_US
dc.titleUp-regulation of airway smooth muscle histamine H1 receptor mRNA, protein, and function by β2-adrenoceptor activationen_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.pmid10779367-
dc.identifier.scopuseid_2-s2.0-0034056415en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0034056415&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume57en_US
dc.identifier.issue5en_US
dc.identifier.spage857en_US
dc.identifier.epage864en_US
dc.identifier.isiWOS:000086762100004-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridMak, JCW=7103323094en_US
dc.identifier.scopusauthoridRoffel, AF=7003590196en_US
dc.identifier.scopusauthoridKatsunuma, T=7004760540en_US
dc.identifier.scopusauthoridElzinga, CRS=6701648214en_US
dc.identifier.scopusauthoridZaagsma, J=16489795900en_US
dc.identifier.scopusauthoridBarnes, PJ=36064679400en_US

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