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首页> 外文期刊>Journal of Cellular Physiology >Estrogens and androgens inhibit association of RANKL with the pre-osteoblast membrane through post-translational mechanisms
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Estrogens and androgens inhibit association of RANKL with the pre-osteoblast membrane through post-translational mechanisms

机译：雌激素和雄激素抑制协会RANKL与pre-osteoblast膜翻译后的机制

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摘要

We have recently demonstrated that RUNX2 promoted, and 17-Estradiol (E2) diminished, association of RANKL with the cell membrane in pre-osteoblast cultures. Here we show that, similar to E2, dihydrotestosterone (DHT) diminishes association of RANKL, and transiently transfected GFP-RANKL with the pre-osteoblast membrane without decreasing total RANKL mRNA or protein levels. Diminution of membrane-associated RANKL was accompanied with marked suppression of osteoclast differentiation from co-cultured pre-osteoclasts, even though DHT increased, not decreased, RANKL concentrations in pre-osteoblast conditioned media. A marked decrease in membrane-associated RANKL was observed after 30min of either E2 or DHT treatment, and near-complete inhibition was observed by 1hr, suggesting that the diminution of RANKL membrane association was mediated through non-genomic mechanisms. Further indicating dispensability of nuclear action of estrogen receptor, E2-mediated inhibition of RANKL membrane association was mimicked by an estrogen dendrimer conjugate (EDC) that cannot enter the cell nucleus. Finally, the inhibitory effect of E2 and DHT on RANKL membrane association was counteracted by the MMP inhibitor NNGH, and the effect of E2 (and not DHT) was antagonized by the Src inhibitor SU6656. Taken together, these results suggest that estrogens and androgens inhibit osteoblast-driven osteoclastogenesis through non-genomic mechanism(s) that entail, MMP-mediated RANKL dissociation from the cell membrane.
机译：我们最近表明RUNX2提拔,和17-Estradiol (E2)减少,协会RANKL pre-osteoblast细胞膜文化。二氢睾酮(DHT)减少了协会RANKL和暂时性的转染GFP-RANKL与pre-osteoblast膜减少总RANKL信使核糖核酸或蛋白质水平。膜相关RANKL的减少伴随着显著抑制破骨细胞从培养分化pre-osteoclasts,尽管DHT增加,没有减少,RANKL浓度pre-osteoblast条件媒体。30分钟后观察RANKL E2或二氢睾酮治疗,几乎完全抑制观察到1小时,这表明减少RANKL膜协会调解通过non-genomic机制。指示可宽恕的核行动的雌激素受体,E2-mediated抑制RANKL膜协会是一个模仿的雌激素聚合物共轭(EDC)不能进入细胞核。E2和RANKL DHT膜的影响协会由MMP抑制剂中和NNGH, E2(而不是DHT)的影响由Src抑制剂SU6656得罪了。在一起,这些结果表明,雌激素和雄激素抑制osteoblast-driven通过non-genomic osteoclastogenesis机制(s),需要MMP-mediated RANKL细胞膜的分离。

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