File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Elevated plasma TGF-β 1 levels in patients with chronic obstructive pulmonary disease

TitleElevated plasma TGF-β 1 levels in patients with chronic obstructive pulmonary disease
Authors
KeywordsChronic obstructive pulmonary disease
Genetic polymorphism
Plasma
Transforming growth factor-β1
Issue Date2009
PublisherElsevier Ltd. The Journal's web site is located at http://www.elsevier.com/locate/rmed
Citation
Respiratory Medicine, 2009, v. 103 n. 7, p. 1083-1089 How to Cite?
AbstractBackground: Transforming growth factor-β 1 (TGF-β 1), a multifunctional cytokine, has been implicated to be responsible for the increased deposition of extracellular matrix in the airways, and increased submucosal collagen expression in chronic obstructive pulmonary disease (COPD). We determined plasma TGF-β 1 levels in patients with COPD and explored its association with common functional polymorphisms of TGF-β 1 gene at C-509T and T869C in the development of COPD in a case-control study. Methods: Stable COPD patients who were ever smokers, and age and pack-years smoked matched healthy controls (n = 205 in each group) were recruited for measurement of plasma TGF-β 1 levels using commercially available ELISA kit, and genotyped at C-509T and T869C functional polymorphisms of TGF-β 1 gene using polymerase chain reaction and restriction fragment length polymorphism (PCR-RFLP). Results: COPD patients had significantly elevated plasma TGF-β 1 levels in comparison to healthy controls irrespective of the genotypes. Allele frequencies and genotype distributions at both polymorphic sites were not different among COPD patients or controls. TGF-β 1 levels were inversely correlated (Pearson's correlation analysis) with FEV 1 (% predicted) (p < 0.001) and FVC (% predicted) (p < 0.001). Conclusion: The findings of elevated plasma TGF-β 1 levels in patients with COPD suggest that TGF-β 1 may play a role in COPD pathogenesis. The C-509T and T869C functional polymorphisms of TGF-β 1 gene do not represent a genetic predisposition to COPD susceptibility in Hong Kong Chinese patients. © 2009 Elsevier Ltd. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/163254
ISSN
2023 Impact Factor: 3.5
2023 SCImago Journal Rankings: 1.180
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorMak, JCWen_US
dc.contributor.authorChan-Yeung, MMWen_US
dc.contributor.authorHo, SPen_US
dc.contributor.authorChan, KSen_US
dc.contributor.authorChoo, Ken_US
dc.contributor.authorYee, KSen_US
dc.contributor.authorChau, CHen_US
dc.contributor.authorCheung, AHKen_US
dc.contributor.authorIp, MSMen_US
dc.date.accessioned2012-09-05T05:29:12Z-
dc.date.available2012-09-05T05:29:12Z-
dc.date.issued2009en_US
dc.identifier.citationRespiratory Medicine, 2009, v. 103 n. 7, p. 1083-1089en_US
dc.identifier.issn0954-6111en_US
dc.identifier.urihttp://hdl.handle.net/10722/163254-
dc.description.abstractBackground: Transforming growth factor-β 1 (TGF-β 1), a multifunctional cytokine, has been implicated to be responsible for the increased deposition of extracellular matrix in the airways, and increased submucosal collagen expression in chronic obstructive pulmonary disease (COPD). We determined plasma TGF-β 1 levels in patients with COPD and explored its association with common functional polymorphisms of TGF-β 1 gene at C-509T and T869C in the development of COPD in a case-control study. Methods: Stable COPD patients who were ever smokers, and age and pack-years smoked matched healthy controls (n = 205 in each group) were recruited for measurement of plasma TGF-β 1 levels using commercially available ELISA kit, and genotyped at C-509T and T869C functional polymorphisms of TGF-β 1 gene using polymerase chain reaction and restriction fragment length polymorphism (PCR-RFLP). Results: COPD patients had significantly elevated plasma TGF-β 1 levels in comparison to healthy controls irrespective of the genotypes. Allele frequencies and genotype distributions at both polymorphic sites were not different among COPD patients or controls. TGF-β 1 levels were inversely correlated (Pearson's correlation analysis) with FEV 1 (% predicted) (p < 0.001) and FVC (% predicted) (p < 0.001). Conclusion: The findings of elevated plasma TGF-β 1 levels in patients with COPD suggest that TGF-β 1 may play a role in COPD pathogenesis. The C-509T and T869C functional polymorphisms of TGF-β 1 gene do not represent a genetic predisposition to COPD susceptibility in Hong Kong Chinese patients. © 2009 Elsevier Ltd. All rights reserved.en_US
dc.languageengen_US
dc.publisherElsevier Ltd. The Journal's web site is located at http://www.elsevier.com/locate/rmeden_US
dc.relation.ispartofRespiratory Medicineen_US
dc.subjectChronic obstructive pulmonary disease-
dc.subjectGenetic polymorphism-
dc.subjectPlasma-
dc.subjectTransforming growth factor-β1-
dc.subject.meshAgeden_US
dc.subject.meshAsian Continental Ancestry Groupen_US
dc.subject.meshCase-Control Studiesen_US
dc.subject.meshFemaleen_US
dc.subject.meshForced Expiratory Volume - Physiologyen_US
dc.subject.meshGenotypeen_US
dc.subject.meshHong Kong - Epidemiologyen_US
dc.subject.meshHumansen_US
dc.subject.meshMaleen_US
dc.subject.meshPolymorphism, Geneticen_US
dc.subject.meshPulmonary Disease, Chronic Obstructive - Blood - Genetics - Physiopathologyen_US
dc.subject.meshSmoking - Geneticsen_US
dc.subject.meshTransforming Growth Factor Beta1 - Blood - Geneticsen_US
dc.titleElevated plasma TGF-β 1 levels in patients with chronic obstructive pulmonary diseaseen_US
dc.typeArticleen_US
dc.identifier.emailMak, JCW:judymak@hku.hken_US
dc.identifier.emailIp, MSM:msmip@hku.hken_US
dc.identifier.authorityMak, JCW=rp00352en_US
dc.identifier.authorityIp, MSM=rp00347en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/j.rmed.2009.01.005en_US
dc.identifier.pmid19186046-
dc.identifier.scopuseid_2-s2.0-67349222280en_US
dc.identifier.hkuros157372-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-67349222280&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume103en_US
dc.identifier.issue7en_US
dc.identifier.spage1083en_US
dc.identifier.epage1089en_US
dc.identifier.isiWOS:000267771900017-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridMak, JCW=7103323094en_US
dc.identifier.scopusauthoridChan-Yeung, MMW=54790582200en_US
dc.identifier.scopusauthoridHo, SP=12794365900en_US
dc.identifier.scopusauthoridChan, KS=7406031627en_US
dc.identifier.scopusauthoridChoo, K=23391819100en_US
dc.identifier.scopusauthoridYee, KS=8139537900en_US
dc.identifier.scopusauthoridChau, CH=7102320975en_US
dc.identifier.scopusauthoridCheung, AHK=12795914100en_US
dc.identifier.scopusauthoridIp, MSM=7102423259en_US
dc.customcontrol.immutablejt 130527-
dc.identifier.issnl0954-6111-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats