File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Down-regulation of aquaporin 3 in bronchiectatic airways in vivo

TitleDown-regulation of aquaporin 3 in bronchiectatic airways in vivo
Authors
KeywordsAquaporins
Bronchial biopsy
Bronchiectasis
Immunohistochemistry
Mucus
Issue Date2003
PublisherElsevier Ltd. The Journal's web site is located at http://www.elsevier.com/locate/rmed
Citation
Respiratory Medicine, 2003, v. 97 n. 1, p. 59-64 How to Cite?
AbstractBronchiectasis is characterized pathologically by permanent abnormal bronchial dilation, and clinically by chronic sputum production. Aquaporin 3 (AQP3), a recently described water channel that is also found in large airway cell membrane, could play a role in the pathogenesis and particularly that of bronchorrhea in bronchiectasis. However, little is known of its in vivo distribution and physiological role in human airways. We have, therefore, performed this quantitative immunohistochemistry study on endobronchial biopsies to evaluate the expression and clinical relevance of AQP3 in patients with idiopathic bronchiectasis (n = 25, 15 F, 64.3 ± 11.5 years) and control subjects (n = 14, 5 F, 57.5 ± 12.0 years). Quantitative image analysis was performed to evaluate the expression of AQP3 in the bronchial epithelial cells. Our results show that AQP3 was predominantly expressed in the basal cells of the epithelial layer in both groups. Expression of AQP3 was significantly reduced in the basal, but not columnar, epithelial cells in bronchiectasis compared with control airways (p = 0.02, 0.35). Only bronchiectatic patients with regular sputum production, but not their counterparts, had significant downregulation of epithelial AQP3 expression compared with control airways (p = 0.004, 0.24). Our findings suggest that AQP3 could have an important role in the pathogenesis of increased mucus production in bronchiectasis. © 2002 Elsevier Science Ltd. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/67953
ISSN
2021 Impact Factor: 4.582
2020 SCImago Journal Rankings: 1.316
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorTsang, KWen_HK
dc.contributor.authorLeung, JCen_HK
dc.contributor.authorTipoe, GLen_HK
dc.contributor.authorLeung, Ren_HK
dc.contributor.authorYan, Cen_HK
dc.contributor.authorOoi, GCen_HK
dc.contributor.authorChan, HHen_HK
dc.contributor.authorLam, WKen_HK
dc.contributor.authorLai, KNen_HK
dc.date.accessioned2010-09-06T05:59:46Z-
dc.date.available2010-09-06T05:59:46Z-
dc.date.issued2003en_HK
dc.identifier.citationRespiratory Medicine, 2003, v. 97 n. 1, p. 59-64en_HK
dc.identifier.issn0954-6111en_HK
dc.identifier.urihttp://hdl.handle.net/10722/67953-
dc.description.abstractBronchiectasis is characterized pathologically by permanent abnormal bronchial dilation, and clinically by chronic sputum production. Aquaporin 3 (AQP3), a recently described water channel that is also found in large airway cell membrane, could play a role in the pathogenesis and particularly that of bronchorrhea in bronchiectasis. However, little is known of its in vivo distribution and physiological role in human airways. We have, therefore, performed this quantitative immunohistochemistry study on endobronchial biopsies to evaluate the expression and clinical relevance of AQP3 in patients with idiopathic bronchiectasis (n = 25, 15 F, 64.3 ± 11.5 years) and control subjects (n = 14, 5 F, 57.5 ± 12.0 years). Quantitative image analysis was performed to evaluate the expression of AQP3 in the bronchial epithelial cells. Our results show that AQP3 was predominantly expressed in the basal cells of the epithelial layer in both groups. Expression of AQP3 was significantly reduced in the basal, but not columnar, epithelial cells in bronchiectasis compared with control airways (p = 0.02, 0.35). Only bronchiectatic patients with regular sputum production, but not their counterparts, had significant downregulation of epithelial AQP3 expression compared with control airways (p = 0.004, 0.24). Our findings suggest that AQP3 could have an important role in the pathogenesis of increased mucus production in bronchiectasis. © 2002 Elsevier Science Ltd. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherElsevier Ltd. The Journal's web site is located at http://www.elsevier.com/locate/rmeden_HK
dc.relation.ispartofRespiratory Medicineen_HK
dc.subjectAquaporinsen_HK
dc.subjectBronchial biopsyen_HK
dc.subjectBronchiectasisen_HK
dc.subjectImmunohistochemistryen_HK
dc.subjectMucusen_HK
dc.subject.meshAquaporin 3en_HK
dc.subject.meshAquaporins - metabolismen_HK
dc.subject.meshBronchi - metabolismen_HK
dc.subject.meshBronchiectasis - metabolism - physiopathologyen_HK
dc.subject.meshDown-Regulationen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshForced Expiratory Volume - physiologyen_HK
dc.subject.meshHumansen_HK
dc.subject.meshImmunohistochemistryen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMiddle Ageden_HK
dc.subject.meshVital Capacity - physiologyen_HK
dc.titleDown-regulation of aquaporin 3 in bronchiectatic airways in vivoen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0954-6111&volume=97&issue=1&spage=59&epage=64&date=2003&atitle=Down-regulation+of+aquaporin+3+in+bronchiectatic+airways+in+vivoen_HK
dc.identifier.emailLeung, JC: jckleung@hku.hken_HK
dc.identifier.emailTipoe, GL: tgeorge@hkucc.hku.hken_HK
dc.identifier.emailLai, KN: knlai@hku.hken_HK
dc.identifier.authorityLeung, JC=rp00448en_HK
dc.identifier.authorityTipoe, GL=rp00371en_HK
dc.identifier.authorityLai, KN=rp00324en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1053/rmed.2002.1413en_HK
dc.identifier.pmid12556012-
dc.identifier.scopuseid_2-s2.0-0037232627en_HK
dc.identifier.hkuros79047en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0037232627&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume97en_HK
dc.identifier.issue1en_HK
dc.identifier.spage59en_HK
dc.identifier.epage64en_HK
dc.identifier.isiWOS:000180514900009-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridTsang, KW=7201555024en_HK
dc.identifier.scopusauthoridLeung, JC=7202180349en_HK
dc.identifier.scopusauthoridTipoe, GL=7003550610en_HK
dc.identifier.scopusauthoridLeung, R=7101876102en_HK
dc.identifier.scopusauthoridYan, C=8728540500en_HK
dc.identifier.scopusauthoridOoi, GC=7006176119en_HK
dc.identifier.scopusauthoridChan, HH=24555248900en_HK
dc.identifier.scopusauthoridLam, WK=7203021937en_HK
dc.identifier.scopusauthoridLai, KN=7402135706en_HK
dc.identifier.issnl0954-6111-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats