File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Glucocorticoids induce β2-adrenergic receptor function in human nasal mucosa

TitleGlucocorticoids induce β2-adrenergic receptor function in human nasal mucosa
Authors
Issue Date1997
PublisherAmerican Thoracic Society. The Journal's web site is located at http://ajrccm.atsjournals.org
Citation
American Journal Of Respiratory And Critical Care Medicine, 1997, v. 155 n. 2, p. 704-710 How to Cite?
AbstractGlucocorticoids are hypothesized to induce β2-adrenergic receptors (β2-R) and their functions. The ability of dexamethasone (DEX) in vitro and beclomethasone dipropionate (BDP) in vivo to induce β2-R messenger RNA (mRNA) and function was investigated in human nasal mucosa. In this tissue, albuterol does not stimulate exocytosis either in vivo or in vitro (Mullol and coworkers, 1992). Therefore, induction of β2-R-mediated glandular exocytosis by glucocorticoids was proposed as an unambiguous outcome measure. Human nasal mucosa was cultured for 3 d with and without 1 μM DEX, then challenged with media or 100 μM albuterol. Culture supernatants were collected for measurement of exocytosed glandular products. Explant mRNA was extracted for reverse transcriptase-polymerase chain reaction (RT-PCR), and in situ hybridization of β2-R mRNA performed. In vivo, normal subjects received saline or BDP for 3 d before albuterol nasal provocation. Concentrations of exocytosed products were measured in nasal secretions. RNA was extracted from nasal epithelial scrapings for RT-PCR. In vitro, DEX treatment induced albuterol-mediated glandular exocytosis (p < 0.04), and increased the steady-state β2-R/β-actin mRNA ratio (p < 0.05), and expression of β2-R mRNA in glands. In vivo, BDP increased the β2-R/β- actin mRNA ratio in epithelial scrapings (p < 0.04), but did not induce albuterol-mediated glandular secretion. We conclude that glucocorticoids increase steady-state β2-R mRNA levels in vivo and in vitro, and can induce β2-R function as assessed by submucosal gland exocytosis in vitro. While topical BDP induced epithelial β2-R mRNA, it did not modulate exocytosis from the deeper submucosal glands.
Persistent Identifierhttp://hdl.handle.net/10722/162170
ISSN
2015 Impact Factor: 13.118
2015 SCImago Journal Rankings: 5.832
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorBaraniuk, JNen_US
dc.contributor.authorAli, Men_US
dc.contributor.authorBrody, Den_US
dc.contributor.authorManiscalco, Jen_US
dc.contributor.authorGaumond, Een_US
dc.contributor.authorFitzgerald, Ten_US
dc.contributor.authorWong, Gen_US
dc.contributor.authorYuta, Aen_US
dc.contributor.authorMak, JCWen_US
dc.contributor.authorBarnes, PJen_US
dc.contributor.authorBascom, Ren_US
dc.contributor.authorTroost, Ten_US
dc.date.accessioned2012-09-05T05:17:47Z-
dc.date.available2012-09-05T05:17:47Z-
dc.date.issued1997en_US
dc.identifier.citationAmerican Journal Of Respiratory And Critical Care Medicine, 1997, v. 155 n. 2, p. 704-710en_US
dc.identifier.issn1073-449Xen_US
dc.identifier.urihttp://hdl.handle.net/10722/162170-
dc.description.abstractGlucocorticoids are hypothesized to induce β2-adrenergic receptors (β2-R) and their functions. The ability of dexamethasone (DEX) in vitro and beclomethasone dipropionate (BDP) in vivo to induce β2-R messenger RNA (mRNA) and function was investigated in human nasal mucosa. In this tissue, albuterol does not stimulate exocytosis either in vivo or in vitro (Mullol and coworkers, 1992). Therefore, induction of β2-R-mediated glandular exocytosis by glucocorticoids was proposed as an unambiguous outcome measure. Human nasal mucosa was cultured for 3 d with and without 1 μM DEX, then challenged with media or 100 μM albuterol. Culture supernatants were collected for measurement of exocytosed glandular products. Explant mRNA was extracted for reverse transcriptase-polymerase chain reaction (RT-PCR), and in situ hybridization of β2-R mRNA performed. In vivo, normal subjects received saline or BDP for 3 d before albuterol nasal provocation. Concentrations of exocytosed products were measured in nasal secretions. RNA was extracted from nasal epithelial scrapings for RT-PCR. In vitro, DEX treatment induced albuterol-mediated glandular exocytosis (p < 0.04), and increased the steady-state β2-R/β-actin mRNA ratio (p < 0.05), and expression of β2-R mRNA in glands. In vivo, BDP increased the β2-R/β- actin mRNA ratio in epithelial scrapings (p < 0.04), but did not induce albuterol-mediated glandular secretion. We conclude that glucocorticoids increase steady-state β2-R mRNA levels in vivo and in vitro, and can induce β2-R function as assessed by submucosal gland exocytosis in vitro. While topical BDP induced epithelial β2-R mRNA, it did not modulate exocytosis from the deeper submucosal glands.en_US
dc.languageengen_US
dc.publisherAmerican Thoracic Society. The Journal's web site is located at http://ajrccm.atsjournals.orgen_US
dc.relation.ispartofAmerican Journal of Respiratory and Critical Care Medicineen_US
dc.subject.meshAdministration, Topicalen_US
dc.subject.meshAdrenergic Beta-Agonists - Pharmacologyen_US
dc.subject.meshAdulten_US
dc.subject.meshAlbuterol - Pharmacologyen_US
dc.subject.meshAnti-Inflammatory Agents - Pharmacologyen_US
dc.subject.meshBronchial Provocation Testsen_US
dc.subject.meshCells, Cultureden_US
dc.subject.meshDexamethasone - Pharmacologyen_US
dc.subject.meshFemaleen_US
dc.subject.meshGlucocorticoidsen_US
dc.subject.meshHumansen_US
dc.subject.meshMaleen_US
dc.subject.meshNasal Mucosa - Drug Effects - Metabolism - Pathologyen_US
dc.subject.meshPolymerase Chain Reactionen_US
dc.subject.meshRna, Messenger - Drug Effectsen_US
dc.subject.meshReceptors, Adrenergic, Beta - Drug Effectsen_US
dc.subject.meshUp-Regulationen_US
dc.titleGlucocorticoids induce β2-adrenergic receptor function in human nasal mucosaen_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.doi10.1164/ajrccm.155.2.9032216-
dc.identifier.pmid9032216-
dc.identifier.scopuseid_2-s2.0-0030614484en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0030614484&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume155en_US
dc.identifier.issue2en_US
dc.identifier.spage704en_US
dc.identifier.epage710en_US
dc.identifier.isiWOS:A1997WH87100047-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridBaraniuk, JN=7006822080en_US
dc.identifier.scopusauthoridAli, M=7404486427en_US
dc.identifier.scopusauthoridBrody, D=7005036946en_US
dc.identifier.scopusauthoridManiscalco, J=8091475700en_US
dc.identifier.scopusauthoridGaumond, E=6507451792en_US
dc.identifier.scopusauthoridFitzgerald, T=7101764649en_US
dc.identifier.scopusauthoridWong, G=7402527563en_US
dc.identifier.scopusauthoridYuta, A=6701670964en_US
dc.identifier.scopusauthoridMak, JCW=7103323094en_US
dc.identifier.scopusauthoridBarnes, PJ=36064679400en_US
dc.identifier.scopusauthoridBascom, R=7006714545en_US
dc.identifier.scopusauthoridTroost, T=6602957750en_US

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats