STIMULATION OF PROSTAGLANDIN (PG) F2-ALPHA AND PGE(2) RELEASE BY TUMOR-NECROSIS-FACTOR-ALPHA AND INTERLEUKIN-1-ALPHA IN CULTURED HUMAN LUTEAL-PHASE ENDOMETRIAL CELLS
STIMULATION OF PROSTAGLANDIN (PG) F2-ALPHA AND PGE(2) RELEASE BY TUMOR-NECROSIS-FACTOR-ALPHA AND INTERLEUKIN-1-ALPHA IN CULTURED HUMAN LUTEAL-PHASE ENDOMETRIAL CELLS
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DOI：
10.1093/oxfordjournals.humrep.a135790
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发表时间：
1995-10-01
影响因子：
6.1
通讯作者：
HARPER, MJK
中科院分区：
文献类型：
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作者：
CHEN, DB;YANG, ZM;HARPER, MJK
肿瘤坏死因子- α (tnf - α)和白细胞介素-1 α (IL-1 α)是子宫细胞信号传导的重要介质。前列腺素（PG）与植入过程中发生的子宫内膜血管通透性增加有关。本研究评估了这两种多效性细胞因子对培养的人黄体期子宫内膜腺上皮细胞（GEC）和基质细胞（STC）释放PGF（2 α）和PGE(2)的影响。PGF和PGE的基础释放量在不同细胞类型之间无显著差异，并随着培养天数的增加而显著下降。第3天，基础PG释放量下降到培养第1天的一半。然而，在培养的第3天，两种细胞类型仍然能够对外源花生四烯酸（5 μ M）的添加做出反应，其中GEC的PG释放量提高了7- 10倍，STC的PG释放量适度提高，但在第4天仍然显著。花生四烯酸对PG释放的促进作用可能表明随着培养时间的延长磷脂酶A2的下调。然而，在培养第0天添加花生四烯酸（5 μ M），虽然能显著增加GEC中PG的释放，但对STC没有影响。相比之下，花生四烯酸（5 μ M）与重组人tnf - α (10 μ g rhtnf - α /l)或10 μ g rhtil -1 α /l的联合添加具有协同作用，与花生四烯酸或细胞因子单独相比，显著增加了两种细胞类型的PGF和PGE的释放（尽管GEC比STC反应更明显）。在加入rhtnf - α或rhIL-1 α后的前24小时内，这两种细胞因子以剂量和时间依赖性的方式刺激两种细胞类型的PG释放。环己亚胺（10 μ M）和放线菌素D （10 μ M）均不影响基础PG释放，但均阻断细胞因子诱导的PG释放。这些结果表明，人子宫内膜细胞PG的生物合成存在差异控制，PG的释放可能通过基因激活来调节。
Tumour necrosis factor-alpha (TNF-alpha) and interleukin-1 alpha (IL-1 alpha) are important mediators of cell signalling in the uterus. Prostaglandins (PG) have been implicated in the increase of endometrial vascular permeability which occurs during the implantation process. This study evaluates the effect of these two pleiotropic cytokines on PGF(2 alpha) and PGE(2) release from human luteal phase endometrial glandular epithelial cells (GEC) and stromal cells (STC) in culture. Basal PGF and PGE release did not differ significantly from each other or among cell types, and declined significantly with increasing number of days in culture. On day 3, basal PG release had decreased to half of that on day 1 of culture. However, both cell types were still able to respond to the addition of exogenous arachidonic acid (5 mu M) an day 3 of culture, with PG release by GEC being elevated 7- to 10-fold and by STC moderately, but still significantly, on day 4. The permissive effect of arachidonic acid on the stimulation of PG release may indicate the down-regulation of phospholipase A2 with continued time in culture. However, the addition of arachidonic acid (5 mu M) on day 0 of culture, while able to cause significantly increased PG release from GEC, had no effect on STC. In contrast, the addition of a combination of arachidonic acid (5 mu M), and either recombinant human TNF-alpha (10 mu g rhTNF-alpha/l) or 10 mu g rhIL-1 alpha/l, had a synergistic action and caused the significantly increased release of PGF and PGE from both cell types, compared with that achieved with either arachidonic acid or the cytokine alone (although GEC responded more than STC). During the first 24 h after the addition of rhTNF-alpha or rhIL-1 alpha, both cytokines stimulated PG release from both cell types in a dose- and time-dependent fashion. Neither cycloheximide (10 mu M) nor actinomycin D (10 mu M) affected basal PG release, but both blocked cytokine-induced PG release from both cell types. These results suggest that there is a differential control of human endometrial cell PG biosynthesis, and that PG release may be regulated through gene activation.