Fooyin University Institutional Repository:Item 987654321/16445
English  |  正體中文  |  简体中文  |  全文笔数/总笔数 : 6024/14565 (41%)
造访人次 : 14163354      在线人数 : 251
RC Version 7.0 © Powered By DSPACE, MIT. Enhanced by NTU Library IR team.
搜寻范围 查询小技巧:
  • 您可在西文检索词汇前后加上"双引号",以获取较精准的检索结果
  • 若欲以作者姓名搜寻,建议至进阶搜寻限定作者字段,可获得较完整数据
  • 进阶搜寻
    主页登入上传说明关于FYIR管理 到手机版


    题名: Urotensin II inhibits doxorubicin-induced human umbilical vein endothelial cell death by modulating ATF expression and via the ERK and Akt pathway
    作者: Yen-Ling Chen;Yi-Ting Tsai;Chung-Yi Lee;Chien-Hsing Lee;Chen, Chung-Yi;Chi-Ming Liu;Jin-Jer Chen;Shih-Hurng Loh;Chien-Sung Tsai
    贡献者: 輔英科技大學 保健營養系
    日期: 2014-09-01
    上传时间: 2015-08-24 20:16:09 (UTC+8)
    摘要: Background and Purpose
    Regulation of the homeostasis of vascular endothelium is critical for the processes of vascular remodeling and angiogenesis under physiological and pathological conditions. Urotensin II (U-II), a potent vasoactive peptide, participates in vascular and myocardial remodeling after injury. We investigated the protective effect of U-II on doxorubicin (DOX)-induced apoptosis in cultured human umbilical vein endothelial cells (HUVECs) and the potential mechanisms involved in this process.
    Experimental Approach
    Cultured HUVECs were treated with vehicle, DOX (1 ?M), U-II, or U-II plus DOX. Apoptosis was evaluated by DNA strand break level with TdT-mediated dUTP nick-end labeling (TUNEL) staining. Western blot analysis was employed to determine the related protein expression and flow cytometry assay was used to determine the TUNEL positive cells.
    Key Results
    U-II reduced the quantity of cleaved caspase-3 and cytosol cytochrome c and increased Bcl-2 expression, which results in protecting HUVECs from DOX-induced apoptosis. U-II induced Activating transcription factor 3 (ATF3) at both mRNA and protein levels in U-II-treated cells. Knockdown of ATF3 with ATF3 siRNA significantly reduced ATF3 protein levels and U-II protective effect under DOX-treated condition. U-II downregulated p53 expression in DOX-induced HUVECs apoptosis, and it rapidly activated extracellular signal-regulated protein kinase (ERK) and Akt. The DOX induced change of p53 was not affected by U-II antagonist (urantide) under ATF-3 knockdown. The inhibitory effect of U-II on DOX-increased apoptosis was attenuated by inhibitors of ERK (U0126) and PI3K/Akt (LY294002).
    Conclusion and Implications
    Our observations provide evidence that U-II protects HUVECs from DOX-induced apoptosis. ERK-Akt phosphorylation, ATF3 activation, and p53 downregulation may play a signal-transduction role in this process.
    關聯: PLoS One 9(9),e106812-無
    显示于类别:[保健營養系] 期刊論文


    档案 大小格式浏览次数




    DSpace Software Copyright © 2002-2004  MIT &  Hewlett-Packard  /   Enhanced by   NTU Library IR team Copyright ©   - 回馈