Reactive oxygen species stimulates epithelial mesenchymal transition in normal human epidermal keratinocytes via TGF-beta secretion.

• Material Type: 博士論文
• Title: Reactive oxygen species stimulates epithelial mesenchymal transition in normal human epidermal keratinocytes via TGF-beta secretion.
• Author/Editor: Fukawa, Teruhisa; Kajiya, Hiroshi; Ozeki, Satoru; Ikebe, Tetsuro; Okabe, Koji
• Author Heading: Fukawa, Teruhisa; Kajiya, Hiroshi; Ozeki, Satoru; Ikebe, Tetsuro; Okabe, Koji
• Publication Date: 2014-03-15
• Publication Date (W3CDTF): 2014-03-15
• Alternative Title: Reactive oxygen species stimulates epithelial mesenchymal transition in normal human epidermal keratinocytes via TGF-beta secretion.
• Degree grantor/type: 福岡歯科大学
• Date Granted: 2014-03-15
• Date Granted (W3CDTF): 2014-03-15
• Dissertation Number: 甲第242号
• Degree Type: 博士（歯学）
• Conferring No. (Dissertation): 甲第242号
• Text Language Code: eng
• Subject Heading: Normal human epidermal keratinocyte; Epithelial to mesenchymal transition; Transforming growth factor-b1; Epithelial cadherin; a-smooth muscle actin; Actins; Base Sequence; Biological Markers; Cadherins; Cells, Cultured; DNA Primers; Epithelial-Mesenchymal Transition; Humans; Hydrogen Peroxide; Keratinocytes; MAP Kinase Signaling System; RNA, Messenger; Reactive Oxygen Species; Transcription Factors; Transforming Growth Factor beta; Up-Regulation
• Target Audience: 一般
• Note (General): Epithelial to mesenchymal transition (EMT) plays an important role in tumor progression, and is an early step in carcinogenesis. Although reactive oxygen species (ROS) are known to be implicated in EMT in many tumor cell types, its exact role in EMT initiation in normal human cells, especially epidermal keratinocytes (NHEKs), remains unknown. To clarify whether ROS induce EMT in NHEKs, and to establish how ROS regulate EMT, we examined the effect of hydrogen peroxide (H(2)O(2)) on the expression of molecules involved in EMT and cell morphology in NHEKs. H(2)O(2) altered the expression of EMT biomarkers, including downregulation of epithelial cadherin and upregulation of α-smooth muscle actin, through a transcriptional modulator, Snail1. H(2)O(2) also induced epithelial to fibroblast-like morphological changes, together with upregulation of EMT biomarkers, and promoted phosphorylation of ERK1/2 and JNK in a time-dependent manner. Interestingly, H(2)O(2) stimulated the expression and secretion of TGF-β1 in NHEKs. Exogenous TGF-β1 also induced the expression of EMT biomarkers. In contrast, neutralizing antibody anti-TGF-β1 antibody or inhibitor of TGF-β receptor type I suppressed the expression of EMT biomarkers. Our results suggest that ROS stimulated TGF-β1 secretion and MAPK activation, resulting in EMT initiation in NHEKs.; ELSEVIER
• Persistent ID (NDL): info:ndljp/pid/9479203; https://dl.ndl.go.jp/pid/9479203
• 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): 2015-08-01T14:40:15+09:00
• Date Created (W3CDTF): 2014-12-02
• 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
• Original Material (URI): http://www.sciencedirect.com/science/article/pii/S0014482712002716
• Periodical Title (URI): https://fdc.repo.nii.ac.jp/records/30
• 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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