Reactive oxygen species promotes cellular senescence in normal human epidermal keratinocytes through epigenetic regulation of p16(INK4a.).

• Material Type: 博士論文
• Title: Reactive oxygen species promotes cellular senescence in normal human epidermal keratinocytes through epigenetic regulation of p16(INK4a.).
• Author/Editor: Sasaki, Mina; Kajiya, Hiroshi; Ozeki, Satoru; Okabe, Koji; Ikebe, Tetsuro
• Author Heading: Sasaki, Mina; Kajiya, Hiroshi; Ozeki, Satoru; Okabe, Koji; Ikebe, Tetsuro
• Publication Date: 2015-03-14
• Publication Date (W3CDTF): 2015-03-14
• Alternative Title: Reactive oxygen species promotes cellular senescence in normal human epidermal keratinocytes through epigenetic regulation of p16(INK4a.).
• Degree grantor/type: 福岡歯科大学
• Date Granted: 2015-03-14
• Date Granted (W3CDTF): 2015-03-14
• Dissertation Number: 甲第261号
• Degree Type: 博士（歯学）
• Conferring No. (Dissertation): 甲第261号
• Text Language Code: eng
• Subject Heading: Cellar senescence; Reactive oxygen species; Cyclin-dependent kinase inhibitors; Normal human epidermal keratinocyte; Biological Markers; Cell Aging; Cell Line, Tumor; Cyclin-Dependent Kinase 4; Cyclin-Dependent Kinase Inhibitor p16; DNA Methylation; Epidermis; Epigenesis, Genetic; G1 Phase Cell Cycle Checkpoints; Humans; Hydrogen Peroxide; Keratinocytes; Organ Specificity; Promoter Regions, Genetic; Reactive Oxygen Species; Retinoblastoma Protein; Signal Transduction; beta-Galactosidase
• Target Audience: 一般
• Note (General): Reactive oxygen species (ROS) can cause severe damage to DNA, proteins and lipids in normal cells, contributing to carcinogenesis and various pathological conditions. While cellular senescence arrests the early phase of cell cycle without any detectable telomere loss or dysfunction. ROS is reported to contribute to induction of cellular senescence, as evidence by its premature onset upon treatment with antioxidants or inhibitors of cellular oxidant scavengers. Although cellular senescence is known to be implicated in tumor suppression, it remains unknown whether ROS initially contributed to be cellular senescence in normal human epidermal keratinocytes (NHEK) and their malignant counterparts. To clarify whether ROS induce cellular senescence in NHEKs, we examined the effect of hydrogen peroxide (H2O2) on the expression of cellular senescence-associated molecules in NHEKs, compared to in squamous carcinoma cells (SCCs). Hydrogen peroxide increased the number of cells positive in senescence associated-β-galactosidase (SA-β-Gal) activity in NHEKs, but not SCCs. The expression of cyclin-dependent kinase (CDK) inhibitors, especially p16(INK4a) was upregulated in NHEKs treated with H2O2. Interestingly, H2O2 suppressed the methylation of p16(INK4a), promoter region in NHEKs, but not in SCCs. Hydrogen peroxide also suppressed the expression of phosphorylated Rb and CDK4, resulting in arrest in G0/G1 phase in NHEKs, but not SCCs. Our results indicate that the ROS-induced cellular senescence in NHEKs was caused by the upregulation p16(INK4a) through demethylation in its promoter region, which is not detected in SCCs, suggesting that ROS-induced cellular senescence contributes to tumor suppression of NHEKs.; Biochem Biophys Res Commun. 2014 Sep 26;452(3):622-8. doi: 10.1016/j.bbrc.2014.08.123. Epub 2014 Aug 30.; doi:10.1016/j.bbrc.2014.08.123
• Persistent ID (NDL): info:ndljp/pid/9479214; https://dl.ndl.go.jp/pid/9479214
• 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): 2015-06-09
• 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): Biochem Biophys Res Commun. 2014 Sep 26;452(3):622-8. doi: 10.1016/j.bbrc.2014.08.123. Epub 2014 Aug 30.; http://www.sciencedirect.com/science/article/pii/S0006291X14015563
• Periodical Title (URI): https://fdc.repo.nii.ac.jp/records/42
• 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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