English  |  正體中文  |  简体中文  |  全文筆數/總筆數 : 45422/58598 (78%)
造訪人次 : 2524680      線上人數 : 213
RC Version 7.0 © Powered By DSPACE, MIT. Enhanced by NTU Library IR team.
搜尋範圍 查詢小技巧:
  • 您可在西文檢索詞彙前後加上"雙引號",以獲取較精準的檢索結果
  • 若欲以作者姓名搜尋,建議至進階搜尋限定作者欄位,可獲得較完整資料
  • 進階搜尋
    請使用永久網址來引用或連結此文件: http://libir.tmu.edu.tw/handle/987654321/5539


    題名: 蛇毒蛋白triflavin抑制血管平滑肌細胞PKC的轉移作用
    Inhibitory Effect of Triflavin on Protein Kinase C Translocation in Vascular Smooth Muscle Cells
    作者: 盧孟珊
    Meng-shan, Lu
    貢獻者: 醫學研究所
    關鍵詞: 蛇毒蛋白
    triflavin
    PKC alpha
    disintegrin
    RGD peptides
    日期: 2003
    上傳時間: 2009-09-11 15:35:29 (UTC+8)
    摘要: 血管平滑肌細胞屬於貼附型細胞,在其生長過程中,細胞外基質( Extracellular matrix )扮演重要的角色。細胞生長時,經由integrin receptor(具a、b兩個次單元)接受外在蛋白質如fibronectin的活化,產生局部附著作用( focal adhesion ),與細胞外基質結合,造成平滑肌細胞的延展( cell spreading )。在這一系列作用中,會造成protein kinase C pathway的活化。
    本篇論文探討蛇毒蛋白triflavin,一種含有RGD (Arg-Gly-Asp)胜肽序列,主要功能在與血小板GP IIb/IIIa complex結合達到抑制血小板凝集作用的disintegrin;將其投與入平滑肌細胞後,應會干擾fibronectin與平滑肌細胞之附著情形;並與抗凝血製劑ReoPro® ( Abciximab )對平滑肌細胞和fibronectin附著情形的影響做一比較。藉由細胞免疫染色及共軛聚焦顯微鏡技術的應用,觀察此反應中,protein kinace C family是否受到活化及其分佈情形,證明triflavin與一般已知的人工RGD蛋白序列,對於平滑肌細胞上integrin receptor產生相同的抑制效果。
    Fibronectin刺激造成平滑肌細胞中protein kinase C產生一短暫升高並轉移到附著作用發生處,事先給予RGD peptides可抑制此情形。若改以triflavin事先投與,其對protein kinase C的表現也有明顯的抑制作用;且抑制功效不亞於ReoPro®造成的抑制成果,甚至更好。證明triflavin可成功結合到平滑肌細胞的 integrin上,達到抑制平滑肌細胞生長。
    The extracellular matrix influences the cellular spreading of vascular smooth muscle cells (VSMCs ) via integrin receptors. We know that VSMCs binding to fibronectin activates the protein kinase C (PKC) pathway, causes differential intracellular PKC isoform translocation, and mediates cell spreading. On this study, VSMCs binding to poly-L-lysine was used as control. We used commercial GRGDS peptides and RGES peptides to prove that the PKCa distribution and VSMCs spreading is mediated by integrin activation. Intracellular distribution of PKC isoforms was measured by confocal microscopy. VSMCs binding to fibronectin induced focal adhesion and cell spreading within 30 minutes. Fibronectin induced a PKC isoform translocation to the cell nucleus and to focal adhesions within 30 minutes. In our previous report, triflavin could specifically bind on platelet GP IIb/IIIa receptor. It was a strong and specific disintegrin. Preincubated VSMCs with triflavin, and then measured the PKC distribution by confocal microscope. We observed triflavin inhibit the distribution of the PKC isofroms in VSMCs. It also inhibited the spreading of VSMCs. We compared triflavin with ReoPro®. We could say that the inhibitory effect of triflavin was stronger than ReoPro®.
    資料類型: thesis
    顯示於類別:[醫學科學研究所] 博碩士論文

    文件中的檔案:

    檔案 描述 大小格式瀏覽次數
    摘要.doc33KbMicrosoft Word79檢視/開啟
    摘要.pdf64KbAdobe PDF182檢視/開啟
    摘要.ppt113KbMicrosoft Powerpoint147檢視/開啟
    摘要.ps346KbPostscript52檢視/開啟


    在TMUIR中所有的資料項目都受到原著作權保護.

    TAIR相關文章

    著作權聲明 Copyright Notice
    • 本平台之數位內容為臺北醫學大學所收錄之機構典藏,包含體系內各式學術著作及學術產出。秉持開放取用的精神,提供使用者進行資料檢索、下載與取用,惟仍請適度、合理地於合法範圍內使用本平台之內容,以尊重著作權人之權益。商業上之利用,請先取得著作權人之授權。

      The digital content on this platform is part of the Taipei Medical University Institutional Repository, featuring various academic works and outputs from the institution. It offers free access to academic research and public education for non-commercial use. Please use the content appropriately and within legal boundaries to respect copyright owners' rights. For commercial use, please obtain prior authorization from the copyright owner.

    • 瀏覽或使用本平台,視同使用者已完全接受並瞭解聲明中所有規範、中華民國相關法規、一切國際網路規定及使用慣例,並不得為任何不法目的使用TMUIR。

      By utilising the platform, users are deemed to have fully accepted and understood all the regulations set out in the statement, relevant laws of the Republic of China, all international internet regulations, and usage conventions. Furthermore, users must not use TMUIR for any illegal purposes.

    • 本平台盡力防止侵害著作權人之權益。若發現本平台之數位內容有侵害著作權人權益情事者,煩請權利人通知本平台維護人員([email protected]),將立即採取移除該數位著作等補救措施。

      TMUIR is made to protect the interests of copyright owners. If you believe that any material on the website infringes copyright, please contact our staff([email protected]). We will remove the work from the repository.

    Back to Top
    DSpace Software Copyright © 2002-2004  MIT &  Hewlett-Packard  /   Enhanced by   NTU Library IR team Copyright ©   - 回饋