File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Contribution of upregulated airway endothelin-1 expression to airway smooth muscle and epithelial cell DNA synthesis after repeated allergen exposure of sensitized Brown-Norway rats

TitleContribution of upregulated airway endothelin-1 expression to airway smooth muscle and epithelial cell DNA synthesis after repeated allergen exposure of sensitized Brown-Norway rats
Authors
Issue Date2000
PublisherAmerican Thoracic Society. The Journal's web site is located at http://ajrcmb.atsjournals.org
Citation
American Journal Of Respiratory Cell And Molecular Biology, 2000, v. 23 n. 5, p. 618-625 How to Cite?
AbstractEndothelin-1 is a potent bronchoconstrictor peptide with proinflammatory and growth-promoting properties. After exposure of sensitized Brown-Norway rats to six repeated ovalbumin exposures, there was an increase in pro-endothelin (ET)-1 messenger RNA compared with saline-exposed control rats 24 h after the final exposure (P < 0.01). ET-1 immunoreactivity was increased sixfold in the bronchial epithelium of the larger conducting airways in the repeated allergen-exposed rats (P < 0.001). After repeated allergen exposure, there were increased rates of DNA synthesis in the airway smooth muscle (ASM) cells (P < 0.001) and epithelial cells (P < 0.001) compared with saline-exposed controls, as measured by bromodeoxyuridine incorporation. Treatment with a dual endothelin A and B (ET(A+B)) receptor antagonist caused a significant attenuation in both ASM (P < 0.001) and epithelial cell (P < 0.001) bromodeoxyuridine incorporation compared with the allergen-challenged and vehicle-treated group. The dual ET(A+B) antagonist attenuated eosinophil recruitment into the airways (P < 0.05) but had no significant effect on increased bronchial reactivity to acetylcholine in allergen-exposed rats. Increased levels of ET-1 in the airways may contribute to inflammation and ASM and epithelial cell DNA synthesis after repeated allergen exposure. Such processes may underlie increased proliferation of resident cells leading to airway wall remodeling in asthmatics.
Persistent Identifierhttp://hdl.handle.net/10722/162372
ISSN
2015 Impact Factor: 4.082
2015 SCImago Journal Rankings: 1.622
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorSalmon, Men_US
dc.contributor.authorLiu, YCen_US
dc.contributor.authorMak, JCWen_US
dc.contributor.authorRousell, Jen_US
dc.contributor.authorHuang, TJen_US
dc.contributor.authorHisada, Ten_US
dc.contributor.authorNicklin, PLen_US
dc.contributor.authorFan Chung, Ken_US
dc.date.accessioned2012-09-05T05:19:21Z-
dc.date.available2012-09-05T05:19:21Z-
dc.date.issued2000en_US
dc.identifier.citationAmerican Journal Of Respiratory Cell And Molecular Biology, 2000, v. 23 n. 5, p. 618-625en_US
dc.identifier.issn1044-1549en_US
dc.identifier.urihttp://hdl.handle.net/10722/162372-
dc.description.abstractEndothelin-1 is a potent bronchoconstrictor peptide with proinflammatory and growth-promoting properties. After exposure of sensitized Brown-Norway rats to six repeated ovalbumin exposures, there was an increase in pro-endothelin (ET)-1 messenger RNA compared with saline-exposed control rats 24 h after the final exposure (P < 0.01). ET-1 immunoreactivity was increased sixfold in the bronchial epithelium of the larger conducting airways in the repeated allergen-exposed rats (P < 0.001). After repeated allergen exposure, there were increased rates of DNA synthesis in the airway smooth muscle (ASM) cells (P < 0.001) and epithelial cells (P < 0.001) compared with saline-exposed controls, as measured by bromodeoxyuridine incorporation. Treatment with a dual endothelin A and B (ET(A+B)) receptor antagonist caused a significant attenuation in both ASM (P < 0.001) and epithelial cell (P < 0.001) bromodeoxyuridine incorporation compared with the allergen-challenged and vehicle-treated group. The dual ET(A+B) antagonist attenuated eosinophil recruitment into the airways (P < 0.05) but had no significant effect on increased bronchial reactivity to acetylcholine in allergen-exposed rats. Increased levels of ET-1 in the airways may contribute to inflammation and ASM and epithelial cell DNA synthesis after repeated allergen exposure. Such processes may underlie increased proliferation of resident cells leading to airway wall remodeling in asthmatics.en_US
dc.languageengen_US
dc.publisherAmerican Thoracic Society. The Journal's web site is located at http://ajrcmb.atsjournals.orgen_US
dc.relation.ispartofAmerican Journal of Respiratory Cell and Molecular Biologyen_US
dc.subject.meshAllergens - Administration & Dosageen_US
dc.subject.meshAnimalsen_US
dc.subject.meshDna - Biosynthesisen_US
dc.subject.meshEndothelin-1 - Biosynthesisen_US
dc.subject.meshEpithelial Cells - Metabolism - Pathologyen_US
dc.subject.meshHypersensitivity - Metabolism - Pathologyen_US
dc.subject.meshMuscle, Smooth - Metabolism - Pathologyen_US
dc.subject.meshOvalbumin - Administration & Dosageen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Inbred Bnen_US
dc.subject.meshRespiratory Physiological Phenomenaen_US
dc.subject.meshUp-Regulation - Drug Effectsen_US
dc.titleContribution of upregulated airway endothelin-1 expression to airway smooth muscle and epithelial cell DNA synthesis after repeated allergen exposure of sensitized Brown-Norway ratsen_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.doi10.1165/ajrcmb.23.5.3909-
dc.identifier.pmid11062140-
dc.identifier.scopuseid_2-s2.0-0033746875en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0033746875&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume23en_US
dc.identifier.issue5en_US
dc.identifier.spage618en_US
dc.identifier.epage625en_US
dc.identifier.isiWOS:000165276700006-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridSalmon, M=7102527335en_US
dc.identifier.scopusauthoridLiu, YC=7410230728en_US
dc.identifier.scopusauthoridMak, JCW=7103323094en_US
dc.identifier.scopusauthoridRousell, J=6602560061en_US
dc.identifier.scopusauthoridHuang, TJ=16750036800en_US
dc.identifier.scopusauthoridHisada, T=7004564760en_US
dc.identifier.scopusauthoridNicklin, PL=36778456500en_US
dc.identifier.scopusauthoridFan Chung, K=6602110678en_US

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats