Human retinal pigment epithelial cell proliferation by the combined stimulation of hydroquinone and advanced glycation end-products via up-regulation of VEGF gene.

• Material Type: 博士論文
• ISSN: 2405-5808
• Title: Human retinal pigment epithelial cell proliferation by the combined stimulation of hydroquinone and advanced glycation end-products via up-regulation of VEGF gene.
• Volume: 2
• Author/Editor: Tsujinaka, Hiroki; Itaya-Hironaka, Asako; Yamauchi, Akiyo; Sakuramoto-Tsuchida, Sumiyo; Ota, Hiroyo; Takeda, Maiko; Fujimura, Takanori; Takasawa, Shin; Ogata, Nahoko
• Author Heading: Tsujinaka, Hiroki; Itaya-Hironaka, Asako; Yamauchi, Akiyo; Sakuramoto-Tsuchida, Sumiyo; Ota, Hiroyo; Takeda, Maiko; Fujimura, Takanori; Takasawa, Shin; Ogata, Nahoko
• Publication, Distribution, etc.: Elsevier
• Publication Date: 2015-07; 2
• Publication Date (W3CDTF): 2015-07
• Alternative Title: ヒト網膜色素上皮はヒドロキノンと最終糖化産物の共刺激により、VEGF遺伝子の発現上昇を伴って増殖する
• Periodical title: Biochemistry and biophysics reports
• Degree grantor/type: 奈良県立医科大学
• Date Granted: 2015-11-27
• Date Granted (W3CDTF): 2015-11-27
• Dissertation Number: 甲第640号
• Degree Type: 博士（医学）
• Conferring No. (Dissertation): 甲第640号
• Text Language Code: eng
• Subject Heading: Age-related macular degeneration; Advanced glycation endproduct(s); Hydroquinone; Retinal pigment epithelial cells; Vascular endothelial growth factor
• Target Audience: 一般
• Note (General): type:Thesis; Although recent research showed that advanced glycation endproduct (AGE) and hydroquinone (HQ) are related to the pathogenesis of age-related macular degeneration (AMD), the mechanism how AGE and HQ induce or accelerate AMD remains elusive. In the present study, we examined the effects of AGE and HQ on changes of human retinal pigment epithelial (RPE) cell numbers and found that the viable cell numbers were markedly reduced by HQ by apoptosis and that AGE prevented the decreases of HQ-treated cell numbers by increased replicative DNA synthesis of RPE cells without changing apoptosis. Real-time RT-PCR revealed that vascular endothelial growth factor (VEGF)-A mRNA was increased by HQ treatment and the addition of HQ+AGE resulted in a further increment. The increase of VEGF secretion was confirmed by ELISA, and inhibition of VEGF signaling by chemical inhibitors and small interfering RNA decreased the HQ+AGE-induced increases in RPE cell numbers. The deletion analysis demonstrated that −102 to −43 region was essential for the VEGF-A promoter activation. Site-directed mutaions of specificity protein 1 (SP1) binding sequences in the VEGF-A promoter and RNA interference of SP1 revealed that SP1 is an essential transcription factor for VEGF-A expression. These results indicate that HQ induces RPE cell apoptosis, leading to dry AMD, and suggest that AGE stimulation in addition to HQ enhances VEGF-A transcription via the AGE-receptor for AGE pathway in HQ-damaged cells. As a result, the secreted VEGF acts as an autocrine/paracrine growth factor for RPE and/or adjacent vascular cells, causing wet AMD.; 博士（医学）・甲第640号・平成27年11月27日; Copyright © 2015 The Authors. Published by Elsevier B.V. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).; identifier:Biochemistry and biophysics reports Vol.2 p.123-131(2015 Jul); identifier:24055808; identifier:http://ginmu.naramed-u.ac.jp/dspace/handle/10564/3101; identifier:Biochemistry and biophysics reports, 2: 123-131
• DOI: info:doi/10.1016/j.bbrep.2015.05.005; https://doi.org/info:doi/10.1016/j.bbrep.2015.05.005
• Persistent ID (NDL): info:ndljp/pid/9577780; https://dl.ndl.go.jp/pid/9577780
• 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): 2016-01-05T14:58:43+09:00
• 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/10564/3101
• 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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