Src參與在prostaglandin E2刺激巨噬細胞產生interferon-beta的反應中

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Title:	Src參與在prostaglandin E2刺激巨噬細胞產生interferon-beta的反應中 Src is required for prostaglandin E2-mediated interferon-beta production in macrophages
Authors:	王韋廸;Wei-Di Wang
Contributors:	分子系統生物醫學研究所碩士班
Keywords:	PGE2;IFN-β;Src
Date:	2013-07-29
Issue Date:	2013-10-02 10:55:23 (UTC+8)
Publisher:	中國醫藥大學
Abstract:	巨噬細胞的COX-2表現受到刺激時，會使前列腺素E2 (Prostaglandin E2, PGE2) 濃度隨之增加。PGE2為前列腺素的家族成員之一。已有研究證實PGE2能促進發炎反應 (inflammation)、細胞激素 (cytokines) 的分泌以及血管新生 (angiogenesis)。由於本實驗室先前發現，當TLR3 (toll-like receptor 3) 被dsRNA (double-stranded RNA) 活化時，會使得Src的蛋白表現增加，並且轉錄interferon-beta (ifn-β) 基因，增加IFN-β的量。本研究發現，PGE2可誘導巨噬細胞的Src表現量增加，並提高ifn-β的mRNA 的量。有趣的是，在巨噬細胞高表達的Src 家族成員之一的Lyn，其蛋白表現量並不受PGE2影響。在送入 src siRNA的巨噬細胞，其PGE2 誘增Src的量減少外，PGE2-induced IFN-β也會同時減少；但當Src的表現量回復，則PGE2-induced IFN-β?狴蝡黕_回來。我們的實驗證明，藉影響 IRF3及IRF7的進入細胞核，並於其內累積，Src參與巨噬細胞的PGE2-induced IFN-β。 Accumulated evidence indicates that via induction of COX-2, the production of prostaglandin E2 (PGE2) is increased in activated macrophages. As one of the prostaglandin family member, PGE2 promotes inflammation, secretion of cytokines and angiogenesis. Previously, our laboratory observed enhanced expression and activity of Src was required for generation of interferon beta (IFN-β) in double-stranded RNA (dsRNA)-stimulated macrophages. In this study, we reported that by virtue of elevation of the expression and activity of Src, PGE2 can cause the increment of IFN-β?nin macrophages. This could be evidenced by attenuation of Src decreased nuclear accumulation of IRF3 and IFR7 and IFN-β?nproduction, while re-introduction of Src reversed all these defects. Intriguingly, the expression of Lyn, one of the myeloid Src relatives did not alter in the presence or absence of PGE2. Our findings indicated that PGE2-elicited Src expression and activation resulted in nuclear translocation of IRF3 and IRF7 that ultimately led to INF-β production.
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