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Functional variability of the adenosine A3 receptor (ADORA3) gene polymorphism in aspirin-induced urticaria.

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dc.contributor.authorKim, SH-
dc.contributor.authorNam, EJ-
dc.contributor.authorKim, YK-
dc.contributor.authorYe, YM-
dc.contributor.authorPark, HS-
dc.date.accessioned2011-05-19T01:57:43Z-
dc.date.available2011-05-19T01:57:43Z-
dc.date.issued2010-
dc.identifier.issn0007-0963-
dc.identifier.urihttp://repository.ajou.ac.kr/handle/201003/2639-
dc.description.abstractBACKGROUND: To improve understanding of aspirin hypersensitivity, this study focused on adenosine as a noncyclooxygenase target molecule of aspirin. Adenosine may affect the release of histamine from cutaneous mast cells through a mechanism mediated by the adenosine A3 receptor.



OBJECTIVES: To investigate the genetic contribution of adenosine A3 receptor gene (ADORA3) polymorphisms in the pathogenesis of aspirin-induced urticaria (AIU) in a case-control association study in a Korean population.



METHODS: A case-control association study was performed in 385 patients with AIU and 213 normal controls from a Korean population. The functional variability of genetic polymorphisms in the ADORA3 gene was analysed in in vitro studies that included a luciferase reporter assay and an electrophoretic mobility shift assay (EMSA), and ex vivo studies that included real-time polymerase chain reaction for mRNA expression in peripheral blood mononuclear cells and a histamine release assay.



RESULTS: A significant association of ADORA3 promoter polymorphism at -1050G/T was found with the phenotype of AIU. Patients with AIU showed higher frequency of the haplotype, ht1 (T(-1050) C(-564) ), compared with normal healthy controls. Moreover, ht1 (TC) was found to be a high-transcript haplotype by the luciferase activity assay, and a -564C allele-specific DNA binding protein was found by EMSA. Increased basophil histamine release was noted in subjects who had the high-transcript haplotype, ht1 (TC).



CONCLUSION: These results suggest that the high-transcript haplotype, ht1 (TC), of the ADORA3 gene may contribute to the development of cutaneous hyper-reactivity to aspirin, leading to the clinical presentation of AIU.
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dc.language.isoen-
dc.subject.MESHAdult-
dc.subject.MESHAnti-Inflammatory Agents, Non-Steroidal-
dc.subject.MESHAsian Continental Ancestry Group-
dc.subject.MESHAspirin-
dc.subject.MESHBasophils-
dc.subject.MESHCase-Control Studies-
dc.subject.MESHDrug Hypersensitivity-
dc.subject.MESHElectrophoretic Mobility Shift Assay-
dc.subject.MESHFemale-
dc.subject.MESHGene Frequency-
dc.subject.MESHGenetic Predisposition to Disease-
dc.subject.MESHGenetic Variation-
dc.subject.MESHHistamine-
dc.subject.MESHHumans-
dc.subject.MESHKorea-
dc.subject.MESHMale-
dc.subject.MESHMiddle Aged-
dc.subject.MESHPolymerase Chain Reaction-
dc.subject.MESHPolymorphism, Genetic-
dc.subject.MESHReceptor, Adenosine A2B-
dc.subject.MESHReceptor, Adenosine A3-
dc.subject.MESHUrticaria-
dc.titleFunctional variability of the adenosine A3 receptor (ADORA3) gene polymorphism in aspirin-induced urticaria.-
dc.typeArticle-
dc.identifier.pmid20716228-
dc.identifier.urlhttp://onlinelibrary.wiley.com/resolve/openurl?genre=article&sid=nlm:pubmed&issn=0007-0963&date=2010&volume=163&issue=5&spage=977-
dc.contributor.affiliatedAuthor김, 승현-
dc.contributor.affiliatedAuthor예, 영민-
dc.contributor.affiliatedAuthor박, 해심-
dc.type.localJournal Papers-
dc.identifier.doi10.1111/j.1365-2133.2010.09983.x-
dc.citation.titleThe British journal of dermatology-
dc.citation.volume163-
dc.citation.number5-
dc.citation.date2010-
dc.citation.startPage977-
dc.citation.endPage985-
dc.identifier.bibliographicCitationThe British journal of dermatology, 163(5). : 977-985, 2010-
dc.identifier.eissn1365-2133-
dc.relation.journalidJ000070963-
Appears in Collections:
Journal Papers > Hospital > Clinical Trial Center
Journal Papers > School of Medicine / Graduate School of Medicine > Allergy
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