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- Publisher Website: 10.1016/j.rmed.2009.01.005
- Scopus: eid_2-s2.0-67349222280
- PMID: 19186046
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Article: Elevated plasma TGF-β 1 levels in patients with chronic obstructive pulmonary disease
Title | Elevated plasma TGF-β 1 levels in patients with chronic obstructive pulmonary disease |
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Authors | |
Keywords | Chronic obstructive pulmonary disease Genetic polymorphism Plasma Transforming growth factor-β1 |
Issue Date | 2009 |
Publisher | Elsevier 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? |
Abstract | Background: 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 Identifier | http://hdl.handle.net/10722/163254 |
ISSN | 2023 Impact Factor: 3.5 2023 SCImago Journal Rankings: 1.180 |
ISI Accession Number ID | |
References |
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Mak, JCW | en_US |
dc.contributor.author | Chan-Yeung, MMW | en_US |
dc.contributor.author | Ho, SP | en_US |
dc.contributor.author | Chan, KS | en_US |
dc.contributor.author | Choo, K | en_US |
dc.contributor.author | Yee, KS | en_US |
dc.contributor.author | Chau, CH | en_US |
dc.contributor.author | Cheung, AHK | en_US |
dc.contributor.author | Ip, MSM | en_US |
dc.date.accessioned | 2012-09-05T05:29:12Z | - |
dc.date.available | 2012-09-05T05:29:12Z | - |
dc.date.issued | 2009 | en_US |
dc.identifier.citation | Respiratory Medicine, 2009, v. 103 n. 7, p. 1083-1089 | en_US |
dc.identifier.issn | 0954-6111 | en_US |
dc.identifier.uri | http://hdl.handle.net/10722/163254 | - |
dc.description.abstract | Background: 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.language | eng | en_US |
dc.publisher | Elsevier Ltd. The Journal's web site is located at http://www.elsevier.com/locate/rmed | en_US |
dc.relation.ispartof | Respiratory Medicine | en_US |
dc.subject | Chronic obstructive pulmonary disease | - |
dc.subject | Genetic polymorphism | - |
dc.subject | Plasma | - |
dc.subject | Transforming growth factor-β1 | - |
dc.subject.mesh | Aged | en_US |
dc.subject.mesh | Asian Continental Ancestry Group | en_US |
dc.subject.mesh | Case-Control Studies | en_US |
dc.subject.mesh | Female | en_US |
dc.subject.mesh | Forced Expiratory Volume - Physiology | en_US |
dc.subject.mesh | Genotype | en_US |
dc.subject.mesh | Hong Kong - Epidemiology | en_US |
dc.subject.mesh | Humans | en_US |
dc.subject.mesh | Male | en_US |
dc.subject.mesh | Polymorphism, Genetic | en_US |
dc.subject.mesh | Pulmonary Disease, Chronic Obstructive - Blood - Genetics - Physiopathology | en_US |
dc.subject.mesh | Smoking - Genetics | en_US |
dc.subject.mesh | Transforming Growth Factor Beta1 - Blood - Genetics | en_US |
dc.title | Elevated plasma TGF-β 1 levels in patients with chronic obstructive pulmonary disease | en_US |
dc.type | Article | en_US |
dc.identifier.email | Mak, JCW:judymak@hku.hk | en_US |
dc.identifier.email | Ip, MSM:msmip@hku.hk | en_US |
dc.identifier.authority | Mak, JCW=rp00352 | en_US |
dc.identifier.authority | Ip, MSM=rp00347 | en_US |
dc.description.nature | link_to_subscribed_fulltext | en_US |
dc.identifier.doi | 10.1016/j.rmed.2009.01.005 | en_US |
dc.identifier.pmid | 19186046 | - |
dc.identifier.scopus | eid_2-s2.0-67349222280 | en_US |
dc.identifier.hkuros | 157372 | - |
dc.relation.references | http://www.scopus.com/mlt/select.url?eid=2-s2.0-67349222280&selection=ref&src=s&origin=recordpage | en_US |
dc.identifier.volume | 103 | en_US |
dc.identifier.issue | 7 | en_US |
dc.identifier.spage | 1083 | en_US |
dc.identifier.epage | 1089 | en_US |
dc.identifier.isi | WOS:000267771900017 | - |
dc.publisher.place | United Kingdom | en_US |
dc.identifier.scopusauthorid | Mak, JCW=7103323094 | en_US |
dc.identifier.scopusauthorid | Chan-Yeung, MMW=54790582200 | en_US |
dc.identifier.scopusauthorid | Ho, SP=12794365900 | en_US |
dc.identifier.scopusauthorid | Chan, KS=7406031627 | en_US |
dc.identifier.scopusauthorid | Choo, K=23391819100 | en_US |
dc.identifier.scopusauthorid | Yee, KS=8139537900 | en_US |
dc.identifier.scopusauthorid | Chau, CH=7102320975 | en_US |
dc.identifier.scopusauthorid | Cheung, AHK=12795914100 | en_US |
dc.identifier.scopusauthorid | Ip, MSM=7102423259 | en_US |
dc.customcontrol.immutable | jt 130527 | - |
dc.identifier.issnl | 0954-6111 | - |