지원사업
학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
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연구자들이 자신의 연구와 전문성을 널리 알리고, 새로운 협력의 기회를 만들 수 있는 네트워킹 공간이에요.
논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2020.1
- 수록면
- 122 - 129 (8page)
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초록· 키워드
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Background: Loss-of-function mutations in the filaggrin gene (FLG), which encodes an epidermal protein crucial for the formation of a functional skin barrier, have been identified as a major predisposing factor in the etiopathogenesis of atopic dermatitis (AD). Recent reports of relatively low frequencies of FLG-null mutations among specific ethnic groups with AD necessitated analysis of the epigenetic regulation which may control FLG expression without altering its DNA sequence. Objective: The study aimed to identify DNA methylation- dependent regulation of FLG expression. Methods: Quantitative polymerase chain reaction was performed to determine the restoration of FLG mRNA expression in normal human epidermal keratinocyte (NHEK) cells after treatment with epigenetic modulating agents. Bisulfite genomic sequencing and pyrosequencing analyses of the FLG promoter region were conducted to identify the citical CpG sites relevant to FLG expression. We performed small-scale pilot study for epidermal tissues obtained from Korean patients with severe AD. Results: We here show that DNA methylation in the FLG with non-CpG island promoter is responsible for the transcriptional regulation of FLG in undifferentiated NHEK cells. The methylation frequencies in a single CpG site of the FLG promoter were significantly higher in lesional epidermis than those in matched nonlesional epidermis of subjects with severe AD. Conclusion: Our in vitro and clinical studies point to this unique CpG site as a potential DNA methylation marker of FLG, which can be a promising therapeutic target in the complications of filaggrin-related skin barrier dysfunction as well as in AD.
목차
등록된 정보가 없습니다.
참고문헌 (40)
참고문헌 신청
Brown SJ / 2012 / One remarkable molecule : filaggrin / J Invest Dermatol 132(3 Pt 2):751~762
Elias PM / 2008 / "Outside-to-inside"(and now back to"outside")pathogenic mechanisms in atopic dermatitis / J Invest Dermatol 128:1067~1070
Smith FJ / 2006 / Loss-of-function mutations in the gene encoding filaggrin cause ichthyosis vulgaris / Nat Genet 38:337~342
Palmer CN / 2006 / Common loss-of-function variants of the epidermal barrier protein filaggrin are a major predisposing factor for atopic dermatitis / Nat Genet 38:441~446
Sandilands A / 2007 / Comprehensive analysis of the gene encoding filaggrin uncovers prevalent and rare mutations in ichthyosis vulgaris and atopic eczema / Nat Genet 39:650~654
Elias PM / 2008 / "Outside-to-inside"(and now back to"outside")pathogenic mechanisms in atopic dermatitis / J Invest Dermatol 128:1067~1070
Smith FJ / 2006 / Loss-of-function mutations in the gene encoding filaggrin cause ichthyosis vulgaris / Nat Genet 38:337~342
Palmer CN / 2006 / Common loss-of-function variants of the epidermal barrier protein filaggrin are a major predisposing factor for atopic dermatitis / Nat Genet 38:441~446
Sandilands A / 2007 / Comprehensive analysis of the gene encoding filaggrin uncovers prevalent and rare mutations in ichthyosis vulgaris and atopic eczema / Nat Genet 39:650~654
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