Protective role of Galectin-7 for skin barrier impairment in atopic dermatitis

• Material Type: 博士論文
• ISSN: 0954-7894
• Title: Protective role of Galectin-7 for skin barrier impairment in atopic dermatitis
• Volume: 50 8
• Author/Editor: 馬屋原, 孝恒
• Author Heading: 馬屋原, 孝恒
• Publication, Distribution, etc.: John Wiley and Sons
• Publication Date: 2020-08
• Publication Date (W3CDTF): 2020-08
• Alternative Title: アトピー性皮膚炎における皮膚バリア障害に対するガレクチン-7の保護的役割
• Periodical title: Clinical & Experimental Allergy
• Degree grantor/type: 浜松医科大学
• Date Granted: 2020-12-11
• Date Granted (W3CDTF): 2020-12-11
• Dissertation Number: 甲第850号
• Degree Type: 博士（医学）
• Conferring No. (Dissertation): 甲第850号
• Text Language Code: eng
• Subject Heading: atopic dermatitis; galectin-7; alarmin
• Target Audience: 一般
• Note (General): doctoral; 医学系研究科; Background: Atopic dermatitis (AD) patients have a barrier disorder in association with Th2 dominant skin inflammation. Galectin-7 (Gal-7), a soluble unglycosylated lectin, is highly expressed in the stratum corneum of AD patients. However, the biological significance of increased Gal-7 expression in AD skin lesions remains unclear.Objective: We aimed to investigate the production mechanism and functional role of Gal-7 in AD patients and IL-4/IL-13-stimulated epidermal keratinocytes.Methods: We assessed the Gal-7 expression levels in skin lesions and sera from AD patients. Gal-7 levels were also measured in monolayered normal human epidermal keratinocytes (NHEKs) and 3-dimensional (3D)-reconstructed epidermis in the presence or absence of IL-4/IL-13 with or without Stat3, Stat6 or Gal-7 gene silencing.Results: Gal-7 was highly expressed in the stratum corneum or intercellular space of AD lesional epidermis as assessed by the stratum corneum proteome analysis and immunohistochemistry. A positive correlation was noted between serum Gal-7 level and transepidermal water loss in patients with AD. These clinical findings were corroborated by our in vitro data, which showed that IL-4/IL-13 facilitated the extracellular release of endogenous Gal-7 in both monolayered NHEKs and 3D-reconstructed epidermis. This machinery was caused by IL-4/IL-13-induced cell damage and inhibited by knockdown of Stat6 but not Stat3 in NHEKs. Moreover, we performed Gal-7 knockdown experiment on 3D-reconstructed epidermis and the result suggested that endogenous Gal-7 serves as a protector from IL-4/IL-13-induced disruption of cell-to-cell adhesion and/or cell-to-extracellular matrix adhesion.Conclusion and Clinical Relevance: Our study unveils the characteristic of Gal-7 and its possible role as an alarmin that reflects the IL-4/IL-13-induced skin barrier impairment in AD.
• DOI: info:doi/10.1111/cea.13672; https://doi.org/info:doi/10.1111/cea.13672
• Persistent ID (NDL): info:ndljp/pid/11710997; https://dl.ndl.go.jp/pid/11710997
• Collection: 障害者向け資料
• Collection (Materials For Handicapped People:1): テキストデータ
• Collection (particular): 国立国会図書館デジタルコレクション > デジタル化資料 > 博士論文; https://dl.ndl.go.jp/collections/A00014
• Acquisition Basis: 博士論文（自動収集）
• Date Accepted (W3CDTF): 2021-08-09T17:15:52+09:00
• Date Created (W3CDTF): 2021-06-08
• Format (IMT): application/pdf
• Access Restrictions: 国立国会図書館内限定公開
• Service for the Digitized Contents Transmission Service: 図書館・個人送信対象外
• Availability of remote photoduplication service: 可
• Periodical Title (URI): http://hdl.handle.net/10271/00003857; https://hama-med.repo.nii.ac.jp/records/3728
• Data Provider (Database): 国立国会図書館 : 国立国会図書館デジタルコレクション; https://dl.ndl.go.jp

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