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Article: Association of urokinase-type plasminogen activator with asthma and atopy

TitleAssociation of urokinase-type plasminogen activator with asthma and atopy
Authors
Issue Date2007
PublisherAmerican Thoracic Society. The Journal's web site is located at http://ajrccm.atsjournals.org
Citation
American Journal of Respiratory and Critical Care Medicine, 2007, v. 175 n. 11, p. 1109-1116 How to Cite?
AbstractRATIONALE: Urokinase plasminogen activator (uPA) interacts with its receptor on inflammatory and migrating cells to regulate extracellular matrix degradation, cell adhesion, and inflammatory cell activation. It is necessary for the development of an appropriate immune response and is involved in tissue remodeling. The PLAU gene codes for this enzyme, and is located on 10q24. This region has demonstrated evidence for linkage in a genome scan for asthma in a sample from northeastern Quebec. Here, we hypothesized that uPA may function as a regulator of asthma susceptibility. OBJECTIVES: To test for association between asthma and genetic variants of PLAU. METHODS: We sequenced PLAU and tested for genetic association between identified variants and asthma-related traits in a French-Canadian familial collection (231 families, 1,139 subjects). Additional association studies were performed in two other family-based Canadian cohorts (Canadian Asthma Primary Prevention Study [CAPPS], 238 trios; and Study of Asthma Genes and the Environment [SAGE], 237 trios). MEASUREMENTS AND MAIN RESULTS: In the original sample, under the dominant model, the common alleles, rs2227564C (P141) and rs2227566T, were associated with asthma (p = 0.011 and 0.045, respectively) and with airway hyperresponsiveness (AHR) (p = 0.026 and 0.038, respectively). Analysis of the linkage disequilibrium pattern also revealed association of the common haplotype for asthma, atopy, and AHR (p = 0.031, 0.043, and 0.006, respectively). Whereas no significant association was detected for PLAU single-nucleotide polymorphisms in the CAPPS cohort, association was observed in the SAGE cohort between the rs4065C allele and atopy under additive (p = 0.005) and dominant (p = 0.0001) genetic models. CONCLUSIONS: This suggests a role for the uPA pathway in the pathogenesis of the disease.
Persistent Identifierhttp://hdl.handle.net/10722/210234
ISSN
2015 Impact Factor: 13.118
2015 SCImago Journal Rankings: 5.832

 

DC FieldValueLanguage
dc.contributor.authorBegin, P-
dc.contributor.authorTremblay, K-
dc.contributor.authorDaley, D-
dc.contributor.authorLemire, M-
dc.contributor.authorClaveau, S-
dc.contributor.authorSalesse, C-
dc.contributor.authorKacel, S-
dc.contributor.authorMontpetit, A-
dc.contributor.authorBecker, A-
dc.contributor.authorChan-Yeung, M-
dc.date.accessioned2015-05-29T07:29:20Z-
dc.date.available2015-05-29T07:29:20Z-
dc.date.issued2007-
dc.identifier.citationAmerican Journal of Respiratory and Critical Care Medicine, 2007, v. 175 n. 11, p. 1109-1116-
dc.identifier.issn1073-449X-
dc.identifier.urihttp://hdl.handle.net/10722/210234-
dc.description.abstractRATIONALE: Urokinase plasminogen activator (uPA) interacts with its receptor on inflammatory and migrating cells to regulate extracellular matrix degradation, cell adhesion, and inflammatory cell activation. It is necessary for the development of an appropriate immune response and is involved in tissue remodeling. The PLAU gene codes for this enzyme, and is located on 10q24. This region has demonstrated evidence for linkage in a genome scan for asthma in a sample from northeastern Quebec. Here, we hypothesized that uPA may function as a regulator of asthma susceptibility. OBJECTIVES: To test for association between asthma and genetic variants of PLAU. METHODS: We sequenced PLAU and tested for genetic association between identified variants and asthma-related traits in a French-Canadian familial collection (231 families, 1,139 subjects). Additional association studies were performed in two other family-based Canadian cohorts (Canadian Asthma Primary Prevention Study [CAPPS], 238 trios; and Study of Asthma Genes and the Environment [SAGE], 237 trios). MEASUREMENTS AND MAIN RESULTS: In the original sample, under the dominant model, the common alleles, rs2227564C (P141) and rs2227566T, were associated with asthma (p = 0.011 and 0.045, respectively) and with airway hyperresponsiveness (AHR) (p = 0.026 and 0.038, respectively). Analysis of the linkage disequilibrium pattern also revealed association of the common haplotype for asthma, atopy, and AHR (p = 0.031, 0.043, and 0.006, respectively). Whereas no significant association was detected for PLAU single-nucleotide polymorphisms in the CAPPS cohort, association was observed in the SAGE cohort between the rs4065C allele and atopy under additive (p = 0.005) and dominant (p = 0.0001) genetic models. CONCLUSIONS: This suggests a role for the uPA pathway in the pathogenesis of the disease.-
dc.languageeng-
dc.publisherAmerican Thoracic Society. The Journal's web site is located at http://ajrccm.atsjournals.org-
dc.relation.ispartofAmerican Journal of Respiratory and Critical Care Medicine-
dc.subject.meshAsthma - enzymology - epidemiology - genetics-
dc.subject.meshDNA - genetics-
dc.subject.meshGene Expression-
dc.subject.meshGenetic Predisposition to Disease-
dc.subject.meshUrokinase-Type Plasminogen Activator - blood - genetics-
dc.titleAssociation of urokinase-type plasminogen activator with asthma and atopy-
dc.typeArticle-
dc.identifier.emailChan-Yeung, M: mmwchan@hku.hk-
dc.identifier.doi10.1164/rccm.200607-1012OC-
dc.identifier.pmid17363771-
dc.identifier.hkuros137440-
dc.identifier.volume175-
dc.identifier.issue11-
dc.identifier.spage1109-
dc.identifier.epage1116-
dc.publisher.placeUnited States-

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