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    題名: 缺氧誘導人類肺部纖維母細胞CXCL12表現之訊息傳遞路徑之探討
    Studies on the signaling pathway in hypoxia-induced CXCL 12 expression in human lung fibroblasts
    作者: 王衍安
    Wang, Yan-An
    關鍵詞: 人類肺部纖維母細胞;肺纖維化;缺氧;CXCR4/CXCL12 (SDF-1);C/EBP?;p300;Akt;Small interfering RNA (siRNA);Dominant-negative mutant (DN);Human lung fibroblast;Idiopathic pulmonary fibrosis;CXCR4/CXCL12 (SDF-1);C/EBP?;p300;Akt;Small interfering RNA (siRNA);Dominant-negative mutant (DN)
    日期: 2014-01-20
    上傳時間: 2019-06-05 11:06:07 (UTC+8)
    摘要: 慢性肺部疾病包括氣喘及源發性肺部纖維化主要的特徵為呼吸道重組、肺纖維化及缺氧的現象。先前的研究指出缺氧在組織纖維化扮演的重要的角色。在慢性氣喘的病人，CXCR4/CXCL12 (stormal cell derived factor-1, SDF-1) 主軸在肺部纖維化扮演著重要的角色。先前的研究指出，在缺氧的刺激下會經由hypoxia-inducible factor-1?悀咮/EBP?狳蚖冗匚XCL12的表現。在本研究中，我們將探討Akt、p300及C/EBP?狾b缺氧誘導人來肺部纖維母細胞CXCL12釋放所扮演的角色。在本研究中我們發現缺氧誘導CXCL12釋放增加會依賴時間及氧氣濃度，也可受到C/EBP?? small interfering RNA (siRNA)、p300抑制劑(anacardia acid)、p300 siRNA及Akt DN 所抑制。缺氧依時間依賴增加C/EBP???n乙醯化、Akt磷酸化、p300磷酸化及HAT的活性。這些結果暗示缺氧誘導人類纖維母細胞CXCL12釋放是透過Akt/p300/C/EBP?狺妍T號傳遞路徑。我們也發現人類肺部纖維母細胞經過缺氧刺激後，其??-smooth muscle actin的表現和細胞的分化有明顯增加。綜合以上結果，本研究首次發現缺氧誘導人類纖維母細胞CXCL12釋放是透過Akt/p300/C/EBP?狺妍T號傳遞路徑。除此之外，缺氧也會誘導人類肺部纖維母細胞分化為肌纖維母細胞。本研究將有助於釐清缺氧造成肺部纖維化之機轉。

    Chronic lung diseases including asthma and idiopathic pulmonary fibrosis (IPF) are characterized by the airway remodeling, lung fibrosis, and hypoxia. Previous study indicated that hypoxia plays a critical role in tissue fibrosis. In chronic asthma, the CXCR4/CXCL12 (stormal-derived factor-1, SDF-1) axis plays an important role in pulmonary fibrosis. Previous study demonstrated that CXCL12 expression is mediated by hypoxia-inducible factor-1?? and C/EBP?? upon hypoxia stimulation. In this study, we further investigated the role of Akt/p300-mediated C/EBP?? acetylation in hypoxia-induced CXCL12 release in human lung fibroblasts. We found that hypoxia-induced increases in CXCL12 release in time- and concentrate-dependent manners. Hypoxia-induced CXCL12 release was inhibited by C/EBP?? small interfering RNA (siRNA), anacardic acid (a p300 inhibitor), p300 siRNA, and dominant negative mutant of Akt (Akt DN). Hypoxia caused time-dependent increase in C/EBP?? acetylation, Akt phosphorylation, p300 phosphorylation, and HAT activity. These results imply that hypoxia-induced increases in CXCL12 release through Akt, p300, and C/EBP?? signaling pathway in human lung fibroblasts. We also found that hypoxia-induced increases ??-smooth muscle actin (??-SMA) expression and cell differentiation in human lung fibroblasts. Taken together, these results suggest that hypoxia-induced CXCL12 expression in human lung fibroblasts through Akt/p300/C/EBP?? signaling pathway. Moreover, hypoxia induced fibroblasts differentiation into myofibroblasts.
    描述: 碩士論文
    委員-黃聰龍
    委員-陳彥州
    指導教授-陳炳常
    資料類型: thesis
    顯示於類別:[醫學檢驗暨生物技術學系所] 博碩士論文

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