Cited 25 times in

Abnormal genetic and epigenetic changes in signal transducer and activator of transcription 4 in the pathogenesis of inflammatory bowel diseases

DC Field Value Language
dc.contributor.author김태일-
dc.contributor.author문창모-
dc.contributor.author천재희-
dc.contributor.author김승원-
dc.contributor.author김원호-
dc.contributor.author김은수-
dc.date.accessioned2014-12-19T16:45:46Z-
dc.date.available2014-12-19T16:45:46Z-
dc.date.issued2012-
dc.identifier.issn0163-2116-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/90146-
dc.description.abstractBACKGROUND AND AIMS: Changes in the expression of signal transducer and activator of transcription 4 (STAT4) contribute to the development of a variety of autoimmune diseases including inflammatory bowel diseases (IBDs). Moreover, epigenetic modifications, including DNA methylation, are considered a basis for differentiation of T helper cells and regulation of cytokines. In this study, we investigated the methylation status of STAT4 gene in IBD patients and the associations between its genetic and epigenetic alterations in IBD patients. METHODS: Blood and colonic mucosa samples were obtained from Korean patients with IBD and healthy controls. Peripheral blood mononuclear cells (PBMCs) were isolated, and total RNA and genomic DNA were isolated from the PBMCs and colon mucosa tissues. The mRNA level and DNA methylation status of the promoter were determined by real-time RT-PCR and pyrosequencing, respectively. The chosen SNPs (rs11889341, rs7574865, rs8179673, rs6752770, rs925847, rs10168266, rs10181656, and rs11685878) were genotyped using the TaqMan nuclease assay. RESULTS: Elevated expression of STAT4 was observed in the colonic mucosa and PBMCs of IBD patients. IBD patients showed a lower degree of methylation of the STAT4 promoter than did the healthy controls. Moreover, a significant correlation between risk alleles and methylation status at -172 of the STAT4 promoter was observed, and mRNA levels of STAT4 in IBD patients were correlated inversely with the T-risk allele (rs7574865). CONCLUSIONS: Our data demonstrated that the DNA methylation status of STAT4 is associated with genetic polymorphisms, providing insights into the interactions between genetic and epigenetic aberrances in STAT4 that contribute to the development of IBD.-
dc.description.statementOfResponsibilityopen-
dc.relation.isPartOfDIGESTIVE DISEASES AND SCIENCES-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHAsian Continental Ancestry Group-
dc.subject.MESHCase-Control Studies-
dc.subject.MESHColon-
dc.subject.MESHDNA/genetics-
dc.subject.MESHDNA Methylation-
dc.subject.MESHGene Expression Regulation/physiology-
dc.subject.MESHGenetic Predisposition to Disease*-
dc.subject.MESHGenotype-
dc.subject.MESHHumans-
dc.subject.MESHInflammatory Bowel Diseases/genetics*-
dc.subject.MESHIntestinal Mucosa-
dc.subject.MESHPolymorphism, Genetic-
dc.subject.MESHPromoter Regions, Genetic-
dc.subject.MESHReal-Time Polymerase Chain Reaction-
dc.subject.MESHReverse Transcriptase Polymerase Chain Reaction-
dc.subject.MESHSTAT4 Transcription Factor/genetics-
dc.subject.MESHSTAT4 Transcription Factor/metabolism*-
dc.titleAbnormal genetic and epigenetic changes in signal transducer and activator of transcription 4 in the pathogenesis of inflammatory bowel diseases-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Internal Medicine (내과학)-
dc.contributor.googleauthorSeung Won Kim-
dc.contributor.googleauthorEun Soo Kim-
dc.contributor.googleauthorChang Mo Moon-
dc.contributor.googleauthorTae Il Kim-
dc.contributor.googleauthorWon Ho Kim-
dc.contributor.googleauthorJae Hee Cheon-
dc.identifier.doi10.1007/s10620-012-2199-z-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA01079-
dc.contributor.localIdA01390-
dc.contributor.localIdA00774-
dc.contributor.localIdA04030-
dc.contributor.localIdA00804-
dc.contributor.localIdA00656-
dc.relation.journalcodeJ00737-
dc.identifier.eissn1573-2568-
dc.identifier.pmid22569826-
dc.identifier.urlhttp://link.springer.com/article/10.1007%2Fs10620-012-2199-z-
dc.subject.keywordSTAT4-
dc.subject.keywordInflammatory bowel disease-
dc.subject.keywordUlcerative colitis-
dc.subject.keywordCrohn’s disease-
dc.subject.keywordIntestinal Bechet’s disease-
dc.subject.keywordDNA methylation-
dc.subject.keywordGenetic polymorphism-
dc.contributor.alternativeNameKim, Tae Il-
dc.contributor.alternativeNameMoon, Chang Mo-
dc.contributor.alternativeNameCheon, Jae Hee-
dc.contributor.alternativeNameKim, Seung Won-
dc.contributor.alternativeNameKim, Won Ho-
dc.contributor.alternativeNameKim, Eun Soo-
dc.contributor.affiliatedAuthorKim, Tae Il-
dc.contributor.affiliatedAuthorMoon, Chang Mo-
dc.contributor.affiliatedAuthorKim, Won Ho-
dc.contributor.affiliatedAuthorCheon, Jae Hee-
dc.contributor.affiliatedAuthorKim, Eun Soo-
dc.contributor.affiliatedAuthorKim, Seung Won-
dc.citation.volume57-
dc.citation.number10-
dc.citation.startPage2600-
dc.citation.endPage2607-
dc.identifier.bibliographicCitationDIGESTIVE DISEASES AND SCIENCES, Vol.57(10) : 2600-2607, 2012-
dc.identifier.rimsid32390-
dc.type.rimsART-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Others (기타) > 1. Journal Papers

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