双S通过激活FSHR和下游cAMP/PKA信号通路,导致过度的雌激素合成
Xiaorong Zhang1,2, Xinda Zhang1, Zhenzhong Zhang1
1College of Marine Life Sciences, Ocean University of China, 266003, Qingdao, Shandong Province, China.
Communications biology
|July 10, 2024
概括
双S暴露会增加雌激素水平,通过与细胞膜上的卵泡刺激激素受体结合. 这激活了一条途径,增强了丸激素转化为17β-雌激醇的途径,从而导致过高雌激素.
科学领域:
- 内分泌学 在内分泌学.
- 环境健康 环境健康
- 分子生物学分子生物学
背景情况:
- 过多的雌激素与女性的各种慢性和急性疾病有关.
- 众所周知,类似雌激素的化合物,如双S,可以增加17β-雌激醇水平,但确切的机制尚不清楚.
研究的目的:
- 为了阐明信号通路,目标部位和参与双S诱导过度雌激素合成的分子.
- 调查环境因素导致高雌激素的分子机制.
主要方法:
- 人类卵巢颗粒细胞 (SVOG) 暴露在1,10和100μg/L的双S度下,持续48小时.
- 对双S积累,受体结合和下游信号通路激活的分析.
主要成果:
- 发现双S主要积聚在细胞膜上.
- 双S与细胞膜上的毛囊刺激激素受体 (FSHR) 结合.
- 观察到循环腺单酸/蛋白激酶A (cAMP/PKA) 途径的激活,导致的转化增加到17β-雌激醇.
结论:
- 双S通过与FSHR结合并激活cAMP/PKA通路而起作用,最终增强雌激素的产生.
- 这项研究提供了关键的洞察力,了解像双S这样的环境因素在过高雌激素的病变发生过程中的作用.
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