國家衛生研究院 NHRI:Item 3990099045/1284
English  |  正體中文  |  简体中文  |  全文筆數/總筆數 : 12145/12927 (94%)
造訪人次 : 857797      線上人數 : 824
RC Version 6.0 © 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
    主頁登入上傳說明關於NHRI管理 到手機版
    請使用永久網址來引用或連結此文件: http://ir.nhri.org.tw/handle/3990099045/1284


    題名: TNF-alpha/IFN-gamma-induced iNOS expression increased by prostaglandin E-2 in rat primary astrocytes via EP2-evoked cAMP/PKA and intracellular calcium signaling
    其他題名: TNF-α/IFN-γ-induced iNOS expression increased by prostaglandin E2 in rat primary astrocytes via EP2-evoked cAMP/PKA and intracellular calcium signaling
    作者: Hsiao, HY;Mak, OT;Yang, CS;Liu, YP;Fang, KM;Tzeng, SF
    貢獻者: Center for Nanomedicine Research
    摘要: Astrocytes, the most abundant glia in the central nervous system (CNS), produce a large amount of prostaglandin E-2 (PGE(2)) in response to proinflammatory mediators after CNS injury. However, it is unclear whether PGE2 has a regulatory role in astrocytic activity under the inflamed condition. In the present work, we showed that PGE2 increased inducible nitric oxide synthase (iNOS) production by tumor necrosis factor-et and interferon-gamma (T/I) in astrocytes. Pharmacological and RNA interference approaches further indicated the involvement of the receptor EP2 in PGE(2)-induced iNOS upregulation in T/I-treated astrocytes. Quantitative real-time polymerase chain reaction and gel mobility shift assays also demonstrated that PGE2 increased iNOS transcription through EP2-induced cAMP/protein kinase A (PYA)-dependent pathway. Consistently, the effect of EP2 was significantly attenuated by the PKA inhibitor KT-5720 and partially suppressed by the inhibitor (SB203580) of p38 mitogen-activated protein kinase (p38MAPK), which serves as one of the downstream components of the PKA-dependent pathway. Interestingly, EP2-mediated PKA signaling appeared to increase intracellular Ca2+ release through inositol triphosphate (IP3) receptor activation, which might in turn stimulate protein kinase C (PKC) activation to promote iNOS production in T/I-primed astrocytes. By analyzing the expression of astrocytic glial fibrillary acidic protein (GFAP), we found that PGE(2) alone only triggered the EP2-induced cAMP/PKA/p38MAPK signaling pathway in astrocytes. Collectively, PGE2 may enhance T/I-induced astrocytic activation by augmenting iNOS/NO production through EP2-mediated cross-talk between cAMP/PKA and IP3/Ca2+ signaling pathways.
    關鍵詞: Neurosciences
    日期: 2007-01-15
    關聯: Glia. 2007 Jan;55(2):214-223.
    Link to: http://dx.doi.org/10.1002/glia.20453
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=0894-1491&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000242629000009
    Cited Times(Scopus): http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=33845914958
    顯示於類別:[楊重熙] 期刊論文

    文件中的檔案:

    檔案 描述 大小格式瀏覽次數
    000242629000009.pdf495KbAdobe PDF1083檢視/開啟


    在NHRI中所有的資料項目都受到原著作權保護.

    TAIR相關文章

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