Full metadata record
DC Field | Value | Language |
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dc.contributor.author | 정일엽 | - |
dc.date.accessioned | 2018-03-08T05:03:44Z | - |
dc.date.available | 2018-03-08T05:03:44Z | - |
dc.date.issued | 2012-04 | - |
dc.identifier.citation | Journal of Human Genetics, APR 2012, 57(4), P.247-253, 7P. | en_US |
dc.identifier.issn | 1434-5161 | - |
dc.identifier.uri | http://www.nature.com/articles/jhg201212 | - |
dc.identifier.uri | http://hdl.handle.net/20.500.11754/43562 | - |
dc.description.abstract | Aspirin-exacerbated respiratory diseases (AERD) are associated with the metabolism of arachidonic acid. FPR2 (formyl peptide receptor2) is a high-affinity ligand receptor for potent anti-inflammatory lipid metabolites: lipoxins. Thus, functional alterations of the FPR2 may contribute to AERD. We investigated the relationship between single-nucleotide polymorphisms (SNPs) in the FPR2 and AERD. Asthmatics were categorized into AERD <15% decreases in forced expiratory volume in one second (FEV1), and/or naso-ocular reactions after oral aspirin challenge (n=170) and aspirin-tolerant asthma (ATA, n=268). In all, 11 SNPs were genotyped. FPR2 protein expressions on CD14-positive monocytes in peripheral blood were measured using flow cytometric analysis. We performed RT-PCR of the FPR2 mRNA expressed by peripheral blood mononuclear cells. Logistic regression analysis showed that the minor allele frequency of FPR2 ?4209T>G (rs1769490) in intron 2 was significantly lower in the AERD group (n=170) than in the ATA group (n=268) (P=0.006, Pcorr=0.04, recessive model). The decline of FEV1 after aspirin challenge was significantly lower in the subjects with GG homozygotes of FPR2 ?4209T>G than those with the other genotypes (P=0.0002). Asthmatic homozygotes for FPR2 ?4209T>G minor allele exhibited significantly higher FPR2 protein expression in CD14-positive monocytes than did those with the common allele of FPR2 ?4209T>G allele (P=0.01). There was no difference in the expression of the wild form and the exon 2 deleted variant form of FPR2 gene according to the genotypes of FPR2 ?4209T>G. The minor allele at FPR2 ?4209T>G may have a protective role against the development of AERD, via increase of FPR2 protein expression in inflammatory cells. | en_US |
dc.description.sponsorship | DNA samples were generously provided by the Soonchunhyang University Bucheon Hospital Biobank, a member of the National Biobank of Korea, supported by the Ministry of Health, Welfare and Family Affairs, Republic of Korea. | en_US |
dc.language.iso | en | en_US |
dc.publisher | Springer Science + Business Media | en_US |
dc.subject | Allergy | en_US |
dc.subject | Genetic association study | en_US |
dc.subject | Genetic variation | en_US |
dc.subject | Respiratory tract diseases | en_US |
dc.title | Association analysis of formyl peptide receptor 2 (FPR2) polymorphisms and Aspirin exacerbated respiratory diseases | en_US |
dc.type | Article | en_US |
dc.relation.no | 4 | - |
dc.relation.volume | 57 | - |
dc.identifier.doi | 10.1038/jhg.2012.12 | - |
dc.relation.page | 247-253 | - |
dc.relation.journal | JOURNAL OF HUMAN GENETICS | - |
dc.contributor.googleauthor | Kim, H. J. | - |
dc.contributor.googleauthor | Cho, S. H. | - |
dc.contributor.googleauthor | Park, J. S. | - |
dc.contributor.googleauthor | Lee, T. H. | - |
dc.contributor.googleauthor | Lee, E. J. | - |
dc.contributor.googleauthor | Kim, Y. H. | - |
dc.contributor.googleauthor | Uh, S. T. | - |
dc.contributor.googleauthor | Chung, I. Y. | - |
dc.contributor.googleauthor | Kim, M. K. | - |
dc.contributor.googleauthor | Choi, I. S. | - |
dc.relation.code | 2012205222 | - |
dc.sector.campus | S | - |
dc.sector.daehak | GRADUATE SCHOOL[S] | - |
dc.sector.department | DEPARTMENT OF BIONANOTECHNOLOGY | - |
dc.identifier.pid | iychu | - |
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