國家衛生研究院 NHRI:Item 3990099045/14055
English  |  正體中文  |  简体中文  |  全文笔数/总笔数 : 12145/12927 (94%)
造访人次 : 853986      在线人数 : 1378
RC Version 6.0 © 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NHRI管理 到手机版


    jsp.display-item.identifier=請使用永久網址來引用或連結此文件: http://ir.nhri.org.tw/handle/3990099045/14055


    题名: Dual specificity phosphatase 6 promotes vascular smooth muscle cell proliferation in response to inflammatary stimulation and vascular injury
    作者: Jiang, WC;Wu, ML;Yet, SF
    贡献者: Institute of Cellular and Systems Medicine
    摘要: Background and Aims: Dual-specificity phosphatases (DUSPs) are protein phosphatases that dephosphorylate tyrosine or serine/threonine residues. DUSP6 dephosphorylates MAPKs in the MAPK pathway, particularly ERK1/2. DUSP6 has been shown to play a critical role in the cellular processes in the heart, diet-induced obesity, T cell differentiation, and endothelial inflammation. However, the functions of DUSP6 in other vascular cells remain to be elucidated. Our goal is to investigate the role of DUSP6 in vascular smooth muscle cells (VSMCs) and in vascular disease.Methods: To examine whether DUSP6 has a role in vascular disease, we performed mouse guide wire injury model. Control and injured arteries were harvested at different time points for histological analysis to asses neointima formation and DUSP6 expression. To evaluate the role of DUSP6 in VSMC proliferation, which contributes to intimal hyperplasia, we performed knockdown and overexpression experiments in VSMCs with or without inflammatory cytokine stimulation. Proliferative activity and ERK1/2 activation were then measured.Results: Immunohistochemistry revealed low level of DUSP6 in normal mouse arteries. In response to injury, DUSP6 expression was increased in the neointima and media layer of the arteries. IL-1b induced DUSP6 level and proliferation in VSMCs. Overexpressing DUSP6 in VSMCs increased cellular proliferation while knocking down DUSP6 with siRNA abrogated IL-1b-induced proliferation. IL-1b-induced ERK1/2 activation preceded DUSP6 induction in VSMCs. Furthermore, ERK1/2 inhibitor abrogated IL-1β-induced ERK1/2 phosphorylation, DUSP6 induction, and VSMC proliferation. Conclusions: Taken together, our results indicate that DUSP6 induction promotes VSMC proliferation and vascular remodeling. DUSP6 might be a therapeutic target for occlusive vascular disease.
    日期: 2020-12-01
    關聯: Atherosclerosis. 2020 Dec;315:E32.
    Link to: http://dx.doi.org/10.1016/j.atherosclerosis.2020.10.108
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=0021-9150&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000748958900090
    显示于类别:[林秀芳] 會議論文/會議摘要

    文件中的档案:

    档案 描述 大小格式浏览次数
    ISI000748958900090.pdf48KbAdobe PDF155检视/开启


    在NHRI中所有的数据项都受到原著作权保护.

    TAIR相关文章

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