Follicle-stimulating hormone promotes age-related endometrial atrophy through cross-talk with transforming growth factor beta signal transduction pathway.
Follicle-stimulating hormone promotes age-related endometrial atrophy through cross-talk with transforming growth factor beta signal transduction pathway.
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卵泡刺激素通过与转化生长因子β信号转导途径的相互作用促进与年龄相关的子宫内膜萎缩
DOI：
10.1111/acel.12278
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发表时间：
2015-04
期刊：
影响因子：
7.8
通讯作者：
Huang H
中科院分区：
文献类型：
--
作者：
Zhang D;Li J;Xu G;Zhang R;Zhou C;Qian Y;Liu Y;Chen L;Zhu B;Ye X;Qu F;Liu X;Shi S;Yang W;Sheng J;Huang H
人们普遍认为，绝经后妇女的子宫内膜萎缩是由于与年龄相关的雌激素水平下降所致。但高循环卵泡刺激素（FSH）在绝经后综合征中的作用尚不清楚。在这里，我们探讨了高循环 FSH 在生理性子宫内膜萎缩中的作用。我们发现 FSH 会加剧小鼠 OVX 后子宫内膜萎缩，并且通过使用促性腺激素释放激素激动剂 (GnRHa) 降低 FSH 可以改善这种效应。在体外，FSH以剂量依赖的方式抑制子宫内膜增殖并促进原代培养的子宫内膜细胞凋亡。此外，子宫内膜腺细胞中还观察到caspase3、caspase8、caspase9、自噬相关蛋白（ATG3、ATG5、ATG7、ATG12和LC3）的上调和c-Jun的下调。此外，smad2 和 smad3 在子宫内膜细胞中表现出时间依赖性激活，可以通过阻断转化生长因子 β 受体 II (TβRII) 来部分抑制这种激活。总之，FSH部分通过激活转化生长因子β（TGFβ）途径影响子宫内膜细胞的增殖、自噬和凋亡来调节子宫内膜萎缩。
It is widely believed that endometrial atrophy in postmenopausal women is due to an age-related reduction in estrogen level. But the role of high circulating follicle-stimulating hormone (FSH) in postmenopausal syndrome is not clear. Here, we explored the role of high circulating FSH in physiological endometrial atrophy. We found that FSH exacerbated post-OVX endometrial atrophy in mice, and this effect was ameliorated by lowering FSH with Gonadotrophin-releasing hormone agonist (GnRHa). In vitro, FSH inhibited endometrial proliferation and promoted the apoptosis of primary cultured endometrial cells in a dose-dependent manner. In addition, upregulation of caspase3, caspase8, caspase9, autophagy-related proteins (ATG3, ATG5, ATG7, ATG12 and LC3) and downregulation of c-Jun were also observed in endometrial adenocytes. Furthermore, smad2 and smad3 showed a time-dependent activation in endometrial cells which can be partly inhibited by blocking the transforming growth factor beta receptor II (TβRII). In conclusion, FSH regulated endometrial atrophy by affecting the proliferation, autophagy and apoptosis of endometrial cells partly through activation of the transforming growth factor beta (TGFβ) pathway.
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影响因子：
3.8
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