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首页> 外文期刊>Life sciences >Estrogen metabolites in the release of inflammatory mediators from human amnion-derived cells.
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Estrogen metabolites in the release of inflammatory mediators from human amnion-derived cells.

机译：雌激素代谢产物从人羊膜来源的细胞释放炎性介质。

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AIMS: Human amnion-derived cells have been used as in vitro models to test the release of inflammatory mediators, such as arachidonic acid (AA) and prostaglandin E(2) (PGE(2)). We compared estrogen metabolites for their ability to induce AA release, to influence PGE(2) production and to interact toward intracellular estrogen receptors (ERs). MAIN METHODS: Metabolite effects on AA and PGE(2) release were examined by radiolabelled substrate incorporation and by colorimetric enzyme immunoassays, respectively. [(3)H]17-beta-estradiol binding displacements were performed on Ro-20-1724 treated whole cells. KEY FINDINGS: In WISH cells, estrone, 2-hydroxy-estrone and estriol induced a rapid dose dependent release of AA that was not inhibited by cycloheximide. Estrone and 2-hydroxy-estrone showed biphasic dose-response curves of PGE(2), whereas estriol and 16-alpha-hydroxy-estrone increased PGE(2) levels at high concentrations. 2-methoxy-estrone, 4-hydroxy-estradiol and 4-hydroxy-estrone did not significantly affect PGE(2) release. 2-methoxy-estradiol and 2-hydroxy-estradiol decreased the PGE(2) release. Effects of metabolites on PGE(2) were inhibited by cycloheximide and by the ER antagonist tamoxifen. In AV3 cells PGE(2) production was poorly detectable. On Ro-20-1724 treated WISH cells the K(i) of 17-beta-estradiol was 29.2 +/- 5.4 nM. Estrone, 2-methoxy-estrone and 2-methoxy-estradiol showed similar affinity values. The hydroxyl substituent at position 2, 4 and 16 decreased or markedly increased the affinity for estradiol or estrone derivatives, respectively. SIGNIFICANCE: The estrogen metabolites induced nongenomic effects on AA release from WISH cells. The influence on PGE(2) release was detectable only on WISH cells. These effects appeared genomic and mediated by intracellular ERs, whose properties seemed strongly dependent on intracellular cAMP levels.
机译：目的：人类羊膜来源的细胞已用作体外模型来测试炎性介质的释放，例如花生四烯酸（AA）和前列腺素E（2）（PGE（2））。我们比较了雌激素代谢物诱导AA释放，影响PGE（2）产生以及与细胞内雌激素受体（ER）相互作用的能力。主要方法：分别通过放射性标记的底物掺入法和比色酶免疫法检测代谢产物对AA和PGE（2）释放的影响。 [（3）H]17-β-雌二醇结合置换是在Ro-20-1724处理的全细胞上进行的。主要发现：在WISH细胞中，雌酮，2-羟基雌酮和雌三醇可诱导剂量依赖性的AA快速释放，而环己酰亚胺并未抑制该释放。雌酮和2-羟基雌酮显示PGE（2）的双相剂量反应曲线，而雌三醇和16-α-羟基雌酮在高浓度下增加PGE（2）的水平。 2-甲氧基雌酮，4-羟基雌二醇和4-羟基雌酮不会显着影响PGE（2）释放。 2-甲氧基雌二醇和2-羟基雌二醇降低PGE（2）释放。代谢物对PGE（2）的作用被环己酰亚胺和ER拮抗剂他莫昔芬抑制。在AV3细胞中，PGE（2）的生产很难检测到。在Ro-20-1724处理的WISH细胞上，17-β-雌二醇的K（i）为29.2 +/- 5.4 nM。雌酮，2-甲氧基-雌酮和2-甲氧基-雌二醇显示相似的亲和力值。 2、4和16位的羟基取代基分别降低或显着提高了对雌二醇或雌酮衍生物的亲和力。意义：雌激素代谢产物对WISH细胞AA释放具有非基因组作用。对PGE（2）释放的影响仅在WISH细胞上可以检测到。这些作用似乎是基因组的，并且是由细胞内ER介导的，其性质似乎强烈依赖于细胞内cAMP的水平。

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