國家衛生研究院 NHRI:Item 3990099045/1530
English  |  正體中文  |  简体中文  |  全文笔数/总笔数 : 12145/12927 (94%)
造访人次 : 857829      在线人数 : 835
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/3990099045/1530


    题名: Transforming growth factor-beta 2 inhibition of corneal endothelial proliferation mediated by prostaglandin
    作者: Chen, KH;Hsu, WM;Chiang, CC;Li, YS
    贡献者: Division of Medical Engineering Research
    摘要: Purpose. To determine the influence of Prostaglandin (PG) E2 on transforming growth factor (TGF)-beta2-mediated inhibitory effects on the proliferation of corneal endothelial cells (CE). Methods. The PGE2 and cell proliferation assays were performed using cultured rabbit corneal endothelium. A PGE2-specific enzyme immunoassay was used to check PGE2 synthesis in supernatants of cells cultured with and without added TGF-beta2 and/or indomethacin. To evaluate the inhibitory effects of PGE2 and TGF-beta2 on CE proliferation, the number of cells grown with exogenous PGE2, or TGF-beta2 with or without indomethacin pretreatment was determined. Results. TGF-beta2, 0.5 to 50 ng/ml, increased the PGE2 secretion of CE dose-dependently in a time-dependent manner. Indomethacin (greater than or equal to0.1 mug/ml) inhibited this PGE2 secretion to a low level (around 5-10 ng/ml) in the presence or absence of exogenous TGF-beta2. Both exogenous TGF-beta2 and PGE2 inhibited CE proliferation dose-dependently over a wide range of concentrations. Indomethacin reversed the inhibitory effects of TGF-P2 but not those of exogenous PGE2. In the medium supplemented with indomethacin, even in the presence of 50 ng/ml of TGF-beta2, CE growth did not differ from control cultures. Conclusions. TGF-beta2 stimulates PGE2 synthesis in CE and inhibits CE proliferation in a dose-dependent manner. Indomethacin extinguishes the inhibitory effects of TGF-beta2 on CE proliferation but not the effect of exogenous PGE2. These data suggest that the antiproliferative effects of TGF-beta2 on CE may be possibly due to TGF-beta2-induced synthesis of PG, most likely PGE2.
    关键词: Ophthalmology
    日期: 2003-06
    關聯: Current Eye Research. 2003 Jun;26(6):363-370.
    Link to: http://search.ebscohost.com/login.aspx?direct=true&db=aph&AN=10444031&site=ehost-live
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=0271-3683&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000184398300007
    Cited Times(Scopus): http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=0042167360
    显示于类别:[其他] 期刊論文

    文件中的档案:

    档案 描述 大小格式浏览次数
    000184398300007.pdf1768KbAdobe PDF273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